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论文类型：期刊论文

发表时间：2013-07-30

发表刊物：JOURNAL OF ETHNOPHARMACOLOGY

收录刊物：SCIE、Scopus

卷号：148

期号：3

页面范围：861-868

ISSN号：0378-8741

关键字：Acanthopanax senticosus extract (ASE); Corticosterone; Neurotoxicity; PC12 cells; Antidepressant; Neuroprotective

摘要：Ethnopharmacological relevance: Acanthopanax senticosus, classified into the family of Araliaceae, has been known for thousands of years as a remedy and is used to treat various diseases in traditional Chinese medicine system including hypertension, ischemic heart disease and hepatitis.
   Aim of the study: This study aimed to examine the protective effects of aqueous extract from Acanthopanax senticosus (ASE) on corticosterone-induced neurotoxicity and its possible mechanisms, using PC12 cells as a suitable in vitro model of depression.
   Materials and methods: In this paper, PC12 cells were treated with 200 mu M of corticosterone in the absence or presence of ASE in varying concentrations for 24 h. Then, cell viability was measured by MTT assay. The release amount of lactate dehydrogenase (LDH) was quantified using LDH assay kit. Apoptosis of PC12 cells was measured by Annexin V-FITC and PI labeling. The intracellular Ca2+ content was tested by fluorescent labeling. The mRNA level of brain-derived neurotrophic factor (BDNF) was examined by RT-PCR, and the expression of CAMP response element binding protein (CREB) was determined by western blotting.
   Results: The results showed that treatment with 200 mu M of corticosterone could induce cytotoxicity in PC12 cells. However, different concentrations of ASE (50, 100, 200, and 400 mu g/mL) significantly increased the cell viability, decreased the LDH release, suppressed the apoptosis of PC12 cells, attenuated the intracellular Ca2+ overloading, up-regulated the BDNF mRNA level and CREB protein expression compared with the corresponding corticosterone-treated group.
   Conclusion: The present results suggest that ASE exerts a neuroprotective effect on corticosterone-induced neurotoxicity in PC12 cells, which may be one of the acting mechanisms that accounts for the in vivo antidepressant activity of ASE. (C) 2013 Elsevier Ireland Ltd. All rights reserved.