Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins

Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Teng, Yan [verfasserIn] Zhang, Meng-Qi Wang, Wen Liu, Li-Tao Zhou, Li-Ming Miao, Shi-Kun Wan, Li-Hong

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Compound danshen tablet Spatial memory impairment ChAT RACK1 BDNF

Anmerkung:	© Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC complementary and alternative medicine - London : BioMed Central, 2001, 14(2014), 1 vom: 14. Jan.
Übergeordnetes Werk:	volume:14 ; year:2014 ; number:1 ; day:14 ; month:01

Links:	Volltext

DOI / URN:	10.1186/1472-6882-14-23

Katalog-ID:	SPR028125088

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520			\|a Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins.
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allfields	10.1186/1472-6882-14-23 doi (DE-627)SPR028125088 (SPR)1472-6882-14-23-e DE-627 ger DE-627 rakwb eng Teng, Yan verfasserin aut Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213 Zhang, Meng-Qi aut Wang, Wen aut Liu, Li-Tao aut Zhou, Li-Ming aut Miao, Shi-Kun aut Wan, Li-Hong aut Enthalten in BMC complementary and alternative medicine London : BioMed Central, 2001 14(2014), 1 vom: 14. Jan. (DE-627)331018713 (DE-600)2050429-9 1472-6882 nnns volume:14 year:2014 number:1 day:14 month:01 https://dx.doi.org/10.1186/1472-6882-14-23 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 14 2014 1 14 01
spelling	10.1186/1472-6882-14-23 doi (DE-627)SPR028125088 (SPR)1472-6882-14-23-e DE-627 ger DE-627 rakwb eng Teng, Yan verfasserin aut Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213 Zhang, Meng-Qi aut Wang, Wen aut Liu, Li-Tao aut Zhou, Li-Ming aut Miao, Shi-Kun aut Wan, Li-Hong aut Enthalten in BMC complementary and alternative medicine London : BioMed Central, 2001 14(2014), 1 vom: 14. Jan. (DE-627)331018713 (DE-600)2050429-9 1472-6882 nnns volume:14 year:2014 number:1 day:14 month:01 https://dx.doi.org/10.1186/1472-6882-14-23 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 14 2014 1 14 01
allfields_unstemmed	10.1186/1472-6882-14-23 doi (DE-627)SPR028125088 (SPR)1472-6882-14-23-e DE-627 ger DE-627 rakwb eng Teng, Yan verfasserin aut Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213 Zhang, Meng-Qi aut Wang, Wen aut Liu, Li-Tao aut Zhou, Li-Ming aut Miao, Shi-Kun aut Wan, Li-Hong aut Enthalten in BMC complementary and alternative medicine London : BioMed Central, 2001 14(2014), 1 vom: 14. Jan. (DE-627)331018713 (DE-600)2050429-9 1472-6882 nnns volume:14 year:2014 number:1 day:14 month:01 https://dx.doi.org/10.1186/1472-6882-14-23 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 14 2014 1 14 01
allfieldsGer	10.1186/1472-6882-14-23 doi (DE-627)SPR028125088 (SPR)1472-6882-14-23-e DE-627 ger DE-627 rakwb eng Teng, Yan verfasserin aut Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213 Zhang, Meng-Qi aut Wang, Wen aut Liu, Li-Tao aut Zhou, Li-Ming aut Miao, Shi-Kun aut Wan, Li-Hong aut Enthalten in BMC complementary and alternative medicine London : BioMed Central, 2001 14(2014), 1 vom: 14. Jan. (DE-627)331018713 (DE-600)2050429-9 1472-6882 nnns volume:14 year:2014 number:1 day:14 month:01 https://dx.doi.org/10.1186/1472-6882-14-23 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 14 2014 1 14 01
allfieldsSound	10.1186/1472-6882-14-23 doi (DE-627)SPR028125088 (SPR)1472-6882-14-23-e DE-627 ger DE-627 rakwb eng Teng, Yan verfasserin aut Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License ( Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213 Zhang, Meng-Qi aut Wang, Wen aut Liu, Li-Tao aut Zhou, Li-Ming aut Miao, Shi-Kun aut Wan, Li-Hong aut Enthalten in BMC complementary and alternative medicine London : BioMed Central, 2001 14(2014), 1 vom: 14. Jan. (DE-627)331018713 (DE-600)2050429-9 1472-6882 nnns volume:14 year:2014 number:1 day:14 month:01 https://dx.doi.org/10.1186/1472-6882-14-23 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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_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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 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 14 2014 1 14 01
language	English
source	Enthalten in BMC complementary and alternative medicine 14(2014), 1 vom: 14. Jan. volume:14 year:2014 number:1 day:14 month:01
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institution	findex.gbv.de
topic_facet	Compound danshen tablet Spatial memory impairment ChAT RACK1 BDNF
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authorswithroles_txt_mv	Teng, Yan @@aut@@ Zhang, Meng-Qi @@aut@@ Wang, Wen @@aut@@ Liu, Li-Tao @@aut@@ Zhou, Li-Ming @@aut@@ Miao, Shi-Kun @@aut@@ Wan, Li-Hong @@aut@@
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author	Teng, Yan
spellingShingle	Teng, Yan misc Compound danshen tablet misc Spatial memory impairment misc ChAT misc RACK1 misc BDNF Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
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topic_title	Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins Compound danshen tablet (dpeaa)DE-He213 Spatial memory impairment (dpeaa)DE-He213 ChAT (dpeaa)DE-He213 RACK1 (dpeaa)DE-He213 BDNF (dpeaa)DE-He213
topic	misc Compound danshen tablet misc Spatial memory impairment misc ChAT misc RACK1 misc BDNF
topic_unstemmed	misc Compound danshen tablet misc Spatial memory impairment misc ChAT misc RACK1 misc BDNF
topic_browse	misc Compound danshen tablet misc Spatial memory impairment misc ChAT misc RACK1 misc BDNF
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title	Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
ctrlnum	(DE-627)SPR028125088 (SPR)1472-6882-14-23-e
title_full	Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
author_sort	Teng, Yan
journal	BMC complementary and alternative medicine
journalStr	BMC complementary and alternative medicine
lang_code	eng
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author_browse	Teng, Yan Zhang, Meng-Qi Wang, Wen Liu, Li-Tao Zhou, Li-Ming Miao, Shi-Kun Wan, Li-Hong
container_volume	14
format_se	Elektronische Aufsätze
author-letter	Teng, Yan
doi_str_mv	10.1186/1472-6882-14-23
title_sort	compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
title_auth	Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
abstract	Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Compound Danshen Tablet (CDT), a Traditional Chinese Medicine, has recently been reported to improve spatial cognition in a rat model of Alzheimer’s disease. However, in vivo neuroprotective mechanism of the CDT in models of spatial memory impairment is not yet evaluated. The present study is aimed to elucidate the cellular mechanism of CDT on $ Aβ_{25-35} $-induced cognitive impairment in mice. Methods Mice were randomly divided into 5 groups: the control group (sham operated), the $ Aβ_{25-35} $ treated group, the positive drug group, and large and small dosage of the CDT groups, respectively. CDT was administered at a dose of 0.81 g/kg and 0.405 g/kg for 3 weeks. The mice in the positive drug group were treated with 0.4 mg/kg of Huperzine A, whereas the mice of the control and $ Aβ_{25-35} $ treated groups were administrated orally with equivalent saline. After 7 days of preventive treatment, mice were subjected to lateral ventricle injection of $ Aβ_{25-35} $ to establish the mice model of Alzheimer’s disease. Spatial memory impairment was evaluated by Morris water maze test. Choline acetyltransferase (ChAT) contents in hippocampus and cortex were quantified by ELISA. The levels of cytokines, receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in hippocampus were measured by RT-PCR and ELISA. Results The results showed that $ Aβ_{25-35} $ caused spatial memory impairment as demonstrated by performance in the Morris water maze test. CDT was able to confer a significant improvement in spatial memory, and protect mice from $ Aβ_{25-35} $-induced neurotoxicity. Additionally, CDT also inhibited the increase of TNF-α and IL-6 level, and increased the expression of choline acetyltransferase (ChAT), receptor of activated protein kinase C1 (RACK1) and brain-derived neurotrophic factor (BDNF) in brain as compared to model mice. Conclusion These findings strongly implicate that CDT may be a useful treatment against learning and memory deficits in mice by rescuing imbalance between cytokines and neurotrophins. © Teng et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Compound danshen tablet ameliorated $ aβ_{25-35} $-induced spatial memory impairment in mice via rescuing imbalance between cytokines and neurotrophins
url	https://dx.doi.org/10.1186/1472-6882-14-23
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author2	Zhang, Meng-Qi Wang, Wen Liu, Li-Tao Zhou, Li-Ming Miao, Shi-Kun Wan, Li-Hong
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