Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway

Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Huang, Xiaoying [verfasserIn] He, Yicheng Chen, Yanfan Wu, Peiliang Gui, Di Cai, Hui Chen, Ali Chen, Mayun Dai, Caijun Yao, Dan Wang, Liangxing

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Pulmonary fibrosis Baicalin Adenosine A2a receptor Transforming growth factor-β1 Extracellular signal regulated kinase1/2

Anmerkung:	© The Author(s). 2016

Übergeordnetes Werk:	Enthalten in: BMC pulmonary medicine - London : BioMed Central, 2001, 16(2016), 1 vom: 23. Sept.
Übergeordnetes Werk:	volume:16 ; year:2016 ; number:1 ; day:23 ; month:09

Links:	Volltext

DOI / URN:	10.1186/s12890-016-0294-1

Katalog-ID:	SPR027995070

Internformat


LEADER	01000caa a22002652 4500
001	SPR027995070
003	DE-627
005	20230520003353.0
007	cr uuu---uuuuu
008	201007s2016 xx \|\|\|\|\|o 00\| \|\|eng c
024	7		\|a 10.1186/s12890-016-0294-1 \|2 doi
035			\|a (DE-627)SPR027995070
035			\|a (SPR)s12890-016-0294-1-e
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
100	1		\|a Huang, Xiaoying \|e verfasserin \|4 aut
245	1	0	\|a Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
264		1	\|c 2016
336			\|a Text \|b txt \|2 rdacontent
337			\|a Computermedien \|b c \|2 rdamedia
338			\|a Online-Ressource \|b cr \|2 rdacarrier
500			\|a © The Author(s). 2016
520			\|a Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis.
650		4	\|a Pulmonary fibrosis \|7 (dpeaa)DE-He213
650		4	\|a Baicalin \|7 (dpeaa)DE-He213
650		4	\|a Adenosine A2a receptor \|7 (dpeaa)DE-He213
650		4	\|a Transforming growth factor-β1 \|7 (dpeaa)DE-He213
650		4	\|a Extracellular signal regulated kinase1/2 \|7 (dpeaa)DE-He213
700	1		\|a He, Yicheng \|4 aut
700	1		\|a Chen, Yanfan \|4 aut
700	1		\|a Wu, Peiliang \|4 aut
700	1		\|a Gui, Di \|4 aut
700	1		\|a Cai, Hui \|4 aut
700	1		\|a Chen, Ali \|4 aut
700	1		\|a Chen, Mayun \|4 aut
700	1		\|a Dai, Caijun \|4 aut
700	1		\|a Yao, Dan \|4 aut
700	1		\|a Wang, Liangxing \|4 aut
773	0	8	\|i Enthalten in \|t BMC pulmonary medicine \|d London : BioMed Central, 2001 \|g 16(2016), 1 vom: 23. Sept. \|w (DE-627)335489125 \|w (DE-600)2059871-3 \|x 1471-2466 \|7 nnns
773	1	8	\|g volume:16 \|g year:2016 \|g number:1 \|g day:23 \|g month:09
856	4	0	\|u https://dx.doi.org/10.1186/s12890-016-0294-1 \|z kostenfrei \|3 Volltext
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_SPRINGER
912			\|a SSG-OLC-PHA
912			\|a GBV_ILN_11
912			\|a GBV_ILN_20
912			\|a GBV_ILN_22
912			\|a GBV_ILN_23
912			\|a GBV_ILN_24
912			\|a GBV_ILN_39
912			\|a GBV_ILN_40
912			\|a GBV_ILN_60
912			\|a GBV_ILN_62
912			\|a GBV_ILN_63
912			\|a GBV_ILN_65
912			\|a GBV_ILN_69
912			\|a GBV_ILN_73
912			\|a GBV_ILN_74
912			\|a GBV_ILN_95
912			\|a GBV_ILN_105
912			\|a GBV_ILN_110
912			\|a GBV_ILN_151
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_206
912			\|a GBV_ILN_213
912			\|a GBV_ILN_230
912			\|a GBV_ILN_285
912			\|a GBV_ILN_293
912			\|a GBV_ILN_602
912			\|a GBV_ILN_2003
912			\|a GBV_ILN_2014
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
912			\|a GBV_ILN_4249
912			\|a GBV_ILN_4305
912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 16 \|j 2016 \|e 1 \|b 23 \|c 09

Indexfelder

author_variant	x h xh y h yh y c yc p w pw d g dg h c hc a c ac m c mc c d cd d y dy l w lw
matchkey_str	article:14712466:2016----::aclnteutsloyiidcdumnrfboivadnsnaaeetreaetf
hierarchy_sort_str	2016
publishDate	2016
allfields	10.1186/s12890-016-0294-1 doi (DE-627)SPR027995070 (SPR)s12890-016-0294-1-e DE-627 ger DE-627 rakwb eng Huang, Xiaoying verfasserin aut Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213 He, Yicheng aut Chen, Yanfan aut Wu, Peiliang aut Gui, Di aut Cai, Hui aut Chen, Ali aut Chen, Mayun aut Dai, Caijun aut Yao, Dan aut Wang, Liangxing aut Enthalten in BMC pulmonary medicine London : BioMed Central, 2001 16(2016), 1 vom: 23. Sept. (DE-627)335489125 (DE-600)2059871-3 1471-2466 nnns volume:16 year:2016 number:1 day:23 month:09 https://dx.doi.org/10.1186/s12890-016-0294-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2016 1 23 09
spelling	10.1186/s12890-016-0294-1 doi (DE-627)SPR027995070 (SPR)s12890-016-0294-1-e DE-627 ger DE-627 rakwb eng Huang, Xiaoying verfasserin aut Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213 He, Yicheng aut Chen, Yanfan aut Wu, Peiliang aut Gui, Di aut Cai, Hui aut Chen, Ali aut Chen, Mayun aut Dai, Caijun aut Yao, Dan aut Wang, Liangxing aut Enthalten in BMC pulmonary medicine London : BioMed Central, 2001 16(2016), 1 vom: 23. Sept. (DE-627)335489125 (DE-600)2059871-3 1471-2466 nnns volume:16 year:2016 number:1 day:23 month:09 https://dx.doi.org/10.1186/s12890-016-0294-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2016 1 23 09
allfields_unstemmed	10.1186/s12890-016-0294-1 doi (DE-627)SPR027995070 (SPR)s12890-016-0294-1-e DE-627 ger DE-627 rakwb eng Huang, Xiaoying verfasserin aut Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213 He, Yicheng aut Chen, Yanfan aut Wu, Peiliang aut Gui, Di aut Cai, Hui aut Chen, Ali aut Chen, Mayun aut Dai, Caijun aut Yao, Dan aut Wang, Liangxing aut Enthalten in BMC pulmonary medicine London : BioMed Central, 2001 16(2016), 1 vom: 23. Sept. (DE-627)335489125 (DE-600)2059871-3 1471-2466 nnns volume:16 year:2016 number:1 day:23 month:09 https://dx.doi.org/10.1186/s12890-016-0294-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2016 1 23 09
allfieldsGer	10.1186/s12890-016-0294-1 doi (DE-627)SPR027995070 (SPR)s12890-016-0294-1-e DE-627 ger DE-627 rakwb eng Huang, Xiaoying verfasserin aut Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213 He, Yicheng aut Chen, Yanfan aut Wu, Peiliang aut Gui, Di aut Cai, Hui aut Chen, Ali aut Chen, Mayun aut Dai, Caijun aut Yao, Dan aut Wang, Liangxing aut Enthalten in BMC pulmonary medicine London : BioMed Central, 2001 16(2016), 1 vom: 23. Sept. (DE-627)335489125 (DE-600)2059871-3 1471-2466 nnns volume:16 year:2016 number:1 day:23 month:09 https://dx.doi.org/10.1186/s12890-016-0294-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2016 1 23 09
allfieldsSound	10.1186/s12890-016-0294-1 doi (DE-627)SPR027995070 (SPR)s12890-016-0294-1-e DE-627 ger DE-627 rakwb eng Huang, Xiaoying verfasserin aut Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213 He, Yicheng aut Chen, Yanfan aut Wu, Peiliang aut Gui, Di aut Cai, Hui aut Chen, Ali aut Chen, Mayun aut Dai, Caijun aut Yao, Dan aut Wang, Liangxing aut Enthalten in BMC pulmonary medicine London : BioMed Central, 2001 16(2016), 1 vom: 23. Sept. (DE-627)335489125 (DE-600)2059871-3 1471-2466 nnns volume:16 year:2016 number:1 day:23 month:09 https://dx.doi.org/10.1186/s12890-016-0294-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2016 1 23 09
language	English
source	Enthalten in BMC pulmonary medicine 16(2016), 1 vom: 23. Sept. volume:16 year:2016 number:1 day:23 month:09
sourceStr	Enthalten in BMC pulmonary medicine 16(2016), 1 vom: 23. Sept. volume:16 year:2016 number:1 day:23 month:09
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Pulmonary fibrosis Baicalin Adenosine A2a receptor Transforming growth factor-β1 Extracellular signal regulated kinase1/2
isfreeaccess_bool	true
container_title	BMC pulmonary medicine
authorswithroles_txt_mv	Huang, Xiaoying @@aut@@ He, Yicheng @@aut@@ Chen, Yanfan @@aut@@ Wu, Peiliang @@aut@@ Gui, Di @@aut@@ Cai, Hui @@aut@@ Chen, Ali @@aut@@ Chen, Mayun @@aut@@ Dai, Caijun @@aut@@ Yao, Dan @@aut@@ Wang, Liangxing @@aut@@
publishDateDaySort_date	2016-09-23T00:00:00Z
hierarchy_top_id	335489125
id	SPR027995070
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR027995070</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230520003353.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2016 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12890-016-0294-1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR027995070</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12890-016-0294-1-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Huang, Xiaoying</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2016</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Pulmonary fibrosis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Baicalin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Adenosine A2a receptor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transforming growth factor-β1</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Extracellular signal regulated kinase1/2</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Yicheng</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Yanfan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wu, Peiliang</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gui, Di</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cai, Hui</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Ali</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Mayun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dai, Caijun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Dan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Liangxing</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC pulmonary medicine</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">16(2016), 1 vom: 23. Sept.</subfield><subfield code="w">(DE-627)335489125</subfield><subfield code="w">(DE-600)2059871-3</subfield><subfield code="x">1471-2466</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:16</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:1</subfield><subfield code="g">day:23</subfield><subfield code="g">month:09</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1186/s12890-016-0294-1</subfield><subfield code="z">kostenfrei</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">16</subfield><subfield code="j">2016</subfield><subfield code="e">1</subfield><subfield code="b">23</subfield><subfield code="c">09</subfield></datafield></record></collection>
author	Huang, Xiaoying
spellingShingle	Huang, Xiaoying misc Pulmonary fibrosis misc Baicalin misc Adenosine A2a receptor misc Transforming growth factor-β1 misc Extracellular signal regulated kinase1/2 Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
authorStr	Huang, Xiaoying
ppnlink_with_tag_str_mv	@@773@@(DE-627)335489125
format	electronic Article
delete_txt_mv	keep
author_role	aut aut aut aut aut aut aut aut aut aut aut
collection	springer
remote_str	true
illustrated	Not Illustrated
issn	1471-2466
topic_title	Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway Pulmonary fibrosis (dpeaa)DE-He213 Baicalin (dpeaa)DE-He213 Adenosine A2a receptor (dpeaa)DE-He213 Transforming growth factor-β1 (dpeaa)DE-He213 Extracellular signal regulated kinase1/2 (dpeaa)DE-He213
topic	misc Pulmonary fibrosis misc Baicalin misc Adenosine A2a receptor misc Transforming growth factor-β1 misc Extracellular signal regulated kinase1/2
topic_unstemmed	misc Pulmonary fibrosis misc Baicalin misc Adenosine A2a receptor misc Transforming growth factor-β1 misc Extracellular signal regulated kinase1/2
topic_browse	misc Pulmonary fibrosis misc Baicalin misc Adenosine A2a receptor misc Transforming growth factor-β1 misc Extracellular signal regulated kinase1/2
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	cr
hierarchy_parent_title	BMC pulmonary medicine
hierarchy_parent_id	335489125
hierarchy_top_title	BMC pulmonary medicine
isfreeaccess_txt	true
familylinks_str_mv	(DE-627)335489125 (DE-600)2059871-3
title	Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
ctrlnum	(DE-627)SPR027995070 (SPR)s12890-016-0294-1-e
title_full	Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
author_sort	Huang, Xiaoying
journal	BMC pulmonary medicine
journalStr	BMC pulmonary medicine
lang_code	eng
isOA_bool	true
recordtype	marc
publishDateSort	2016
contenttype_str_mv	txt
author_browse	Huang, Xiaoying He, Yicheng Chen, Yanfan Wu, Peiliang Gui, Di Cai, Hui Chen, Ali Chen, Mayun Dai, Caijun Yao, Dan Wang, Liangxing
container_volume	16
format_se	Elektronische Aufsätze
author-letter	Huang, Xiaoying
doi_str_mv	10.1186/s12890-016-0294-1
title_sort	baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine a2a receptor related tgf-β1-induced erk1/2 signaling pathway
title_auth	Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
abstract	Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. © The Author(s). 2016
abstractGer	Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. © The Author(s). 2016
abstract_unstemmed	Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis. © The Author(s). 2016
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700
container_issue	1
title_short	Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway
url	https://dx.doi.org/10.1186/s12890-016-0294-1
remote_bool	true
author2	He, Yicheng Chen, Yanfan Wu, Peiliang Gui, Di Cai, Hui Chen, Ali Chen, Mayun Dai, Caijun Yao, Dan Wang, Liangxing
author2Str	He, Yicheng Chen, Yanfan Wu, Peiliang Gui, Di Cai, Hui Chen, Ali Chen, Mayun Dai, Caijun Yao, Dan Wang, Liangxing
ppnlink	335489125
mediatype_str_mv	c
isOA_txt	true
hochschulschrift_bool	false
doi_str	10.1186/s12890-016-0294-1
up_date	2024-07-03T16:35:07.130Z
_version_	1803576417591492608
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR027995070</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230520003353.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2016 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s12890-016-0294-1</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR027995070</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12890-016-0294-1-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Huang, Xiaoying</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s). 2016</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Baicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis. Methods The A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. Results Severe lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. Conclusions Genetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Pulmonary fibrosis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Baicalin</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Adenosine A2a receptor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transforming growth factor-β1</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Extracellular signal regulated kinase1/2</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Yicheng</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Yanfan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wu, Peiliang</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gui, Di</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cai, Hui</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Ali</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Mayun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dai, Caijun</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yao, Dan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Liangxing</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC pulmonary medicine</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">16(2016), 1 vom: 23. Sept.</subfield><subfield code="w">(DE-627)335489125</subfield><subfield code="w">(DE-600)2059871-3</subfield><subfield code="x">1471-2466</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:16</subfield><subfield code="g">year:2016</subfield><subfield code="g">number:1</subfield><subfield code="g">day:23</subfield><subfield code="g">month:09</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1186/s12890-016-0294-1</subfield><subfield code="z">kostenfrei</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">16</subfield><subfield code="j">2016</subfield><subfield code="e">1</subfield><subfield code="b">23</subfield><subfield code="c">09</subfield></datafield></record></collection>
score	7.402587

Nicht das Richtige dabei?

Schreiben Sie uns!

Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-β1-induced ERK1/2 signaling pathway

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?