Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway
Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was...
Ausführliche Beschreibung
Autor*in: |
Yuan-Yuan Cao [verfasserIn] Ke Li [verfasserIn] Ying Li [verfasserIn] Xiao-Ting Tian [verfasserIn] Hui-Xue Ba [verfasserIn] Aiping Wang [verfasserIn] Xiao-Hui Li [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2020 |
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Schlagwörter: |
left ventricular systolic pressure |
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Übergeordnetes Werk: |
In: Pharmaceutical Biology - Taylor & Francis Group, 2017, 58(2020), 1, Seite 176-183 |
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Übergeordnetes Werk: |
volume:58 ; year:2020 ; number:1 ; pages:176-183 |
Links: |
Link aufrufen |
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DOI / URN: |
10.1080/13880209.2020.1723648 |
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Katalog-ID: |
DOAJ057878676 |
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520 | |a Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. | ||
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10.1080/13880209.2020.1723648 doi (DE-627)DOAJ057878676 (DE-599)DOAJd5d6967cfa8b4de5843c4ad288491e18 DE-627 ger DE-627 rakwb eng RM1-950 Yuan-Yuan Cao verfasserin aut Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis Therapeutics. Pharmacology Ke Li verfasserin aut Ying Li verfasserin aut Xiao-Ting Tian verfasserin aut Hui-Xue Ba verfasserin aut Aiping Wang verfasserin aut Xiao-Hui Li verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 58(2020), 1, Seite 176-183 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:58 year:2020 number:1 pages:176-183 https://doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/article/d5d6967cfa8b4de5843c4ad288491e18 kostenfrei http://dx.doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 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 58 2020 1 176-183 |
spelling |
10.1080/13880209.2020.1723648 doi (DE-627)DOAJ057878676 (DE-599)DOAJd5d6967cfa8b4de5843c4ad288491e18 DE-627 ger DE-627 rakwb eng RM1-950 Yuan-Yuan Cao verfasserin aut Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis Therapeutics. Pharmacology Ke Li verfasserin aut Ying Li verfasserin aut Xiao-Ting Tian verfasserin aut Hui-Xue Ba verfasserin aut Aiping Wang verfasserin aut Xiao-Hui Li verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 58(2020), 1, Seite 176-183 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:58 year:2020 number:1 pages:176-183 https://doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/article/d5d6967cfa8b4de5843c4ad288491e18 kostenfrei http://dx.doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 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 58 2020 1 176-183 |
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10.1080/13880209.2020.1723648 doi (DE-627)DOAJ057878676 (DE-599)DOAJd5d6967cfa8b4de5843c4ad288491e18 DE-627 ger DE-627 rakwb eng RM1-950 Yuan-Yuan Cao verfasserin aut Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis Therapeutics. Pharmacology Ke Li verfasserin aut Ying Li verfasserin aut Xiao-Ting Tian verfasserin aut Hui-Xue Ba verfasserin aut Aiping Wang verfasserin aut Xiao-Hui Li verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 58(2020), 1, Seite 176-183 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:58 year:2020 number:1 pages:176-183 https://doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/article/d5d6967cfa8b4de5843c4ad288491e18 kostenfrei http://dx.doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 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 58 2020 1 176-183 |
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10.1080/13880209.2020.1723648 doi (DE-627)DOAJ057878676 (DE-599)DOAJd5d6967cfa8b4de5843c4ad288491e18 DE-627 ger DE-627 rakwb eng RM1-950 Yuan-Yuan Cao verfasserin aut Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis Therapeutics. Pharmacology Ke Li verfasserin aut Ying Li verfasserin aut Xiao-Ting Tian verfasserin aut Hui-Xue Ba verfasserin aut Aiping Wang verfasserin aut Xiao-Hui Li verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 58(2020), 1, Seite 176-183 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:58 year:2020 number:1 pages:176-183 https://doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/article/d5d6967cfa8b4de5843c4ad288491e18 kostenfrei http://dx.doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 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 58 2020 1 176-183 |
allfieldsSound |
10.1080/13880209.2020.1723648 doi (DE-627)DOAJ057878676 (DE-599)DOAJd5d6967cfa8b4de5843c4ad288491e18 DE-627 ger DE-627 rakwb eng RM1-950 Yuan-Yuan Cao verfasserin aut Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis Therapeutics. Pharmacology Ke Li verfasserin aut Ying Li verfasserin aut Xiao-Ting Tian verfasserin aut Hui-Xue Ba verfasserin aut Aiping Wang verfasserin aut Xiao-Hui Li verfasserin aut In Pharmaceutical Biology Taylor & Francis Group, 2017 58(2020), 1, Seite 176-183 (DE-627)300595905 (DE-600)1483151-X 17445116 nnns volume:58 year:2020 number:1 pages:176-183 https://doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/article/d5d6967cfa8b4de5843c4ad288491e18 kostenfrei http://dx.doi.org/10.1080/13880209.2020.1723648 kostenfrei https://doaj.org/toc/1388-0209 Journal toc kostenfrei https://doaj.org/toc/1744-5116 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 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_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 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 58 2020 1 176-183 |
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RM1-950 Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway left ventricular systolic pressure heart-to-body weight ratio left ventricular/tibia length extracellular regulated protein kinases h9c2 phalloidin staining cardiac fibrosis |
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dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the erk signalling pathway |
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Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway |
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Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. |
abstractGer |
Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. |
abstract_unstemmed |
Context The pharmacological functions of Dendrobium candidum Wall. ex Lindl. (Orchidaceae) in cardiac hypertrophy remains unclear. Objective To evaluate whether D. candidum aqueous extract (DCAE) can attenuate experimental cardiac hypertrophy. Materials and methods Cardiac hypertrophy in SD rats was induced by subcutaneously injection of isoproterenol (2 mg/kg), once a day for ten days. Rats were gavaged with DCAE (0.13 and 0.78 g/kg) daily for one month. At the end of treatment, measurement of left ventricular systolic pressure (LVSP), heart-to-body weight ratio (HW/BW), left ventricular/tibia length (LV/TL), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) levels, haematoxylin-eosin staining, and Masson’s trichrome staining were conducted. In cultured H9c2 cells, DCAE (2 mg/mL) and U0126 (10 μM) were added 2 h before the isoproterenol (10 μM) stimulus. Phalloidin staining was used to evaluate cellular hypertrophy. The mRNA expression of ANP and BNP was measured by qRT-PCR. The expression of p-ERK was determined by immunoblotting. Results DCAE treatment significantly reduced the following indicators in vivo: (1) the LVSP (16%); (2) HW/BW (13%); (3) LV/TL (6%); (4) ANP (39%); (5) BNP (32%). In cultured H9c2 cells, phalloidin staining showed that DCAE relieved cellular hypertrophy (53% reduction). Furthermore, immunoblotting showed that DCAE can significantly inhibit p-ERK protein expression in vivo and in vitro (39% and 27% reduction, respectively). Discussion and conclusions DCAE prevents cardiac hypertrophy via ERK signalling pathway and has the potential for treatment of cardiac hypertrophy. |
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Dendrobium candidum aqueous extract attenuates isoproterenol-induced cardiac hypertrophy through the ERK signalling pathway |
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