Panax ginseng ginsenoside-Rg2 protects memory impairment via anti-apoptosis in a rat model with vascular dementia.

Authors: Zhang, G  Liu, A  Zhou, Y  San, X  Jin, T  Jin, Y 
Citation: Zhang G, etal., J Ethnopharmacol. 2008 Feb 12;115(3):441-8. Epub 2007 Oct 25.
Pubmed: (View Article at PubMed) PMID:18083315
DOI: Full-text: DOI:10.1016/j.jep.2007.10.026

ETHNOPHARMACOLOGICAL RELEVANCE: Ginsenosides, the major active ingredients of Panax ginseng, produce a variety of pharmacological or physiological responses with effects on the central and peripheral nervous systems. AIM OF THE STUDY: In this report, we investigated the effects of ginsenoside Rg2 on cerebral ischemia-reperfusion induced impairment of neurological responses, memory and caudate-putamen neuronal apoptosis in a vascular dementia (VD) rat model. MATERIALS AND METHODS: Neurological evaluation was performed 24h after reperfusion and Y-maze memory performance was assessed at 48 h after reperfusion. Immunocytochemical techniques were employed to check the protein expression of BCL-2, BAX, heat shock protein 70 and P53, which are related with cell apoptosis. RESULTS: Neurological responses and memory ability of the ginsenoside Rg2 or nimodipine groups improved significantly compared with the VD group. The expression of BCL-2 and HSP70 were decreased, while BAX and P53 were increased in the VD model. The expression of BCL-2 and HSP70 proteins were increased, while BAX and P53 decreased after ginsenoside Rg2 (2.5, 5 and 10mg/kg) and nimodipine (50 microg/kg) treatment compared with the VD group. The study suggests that ginsenoside Rg2 improved neurological performance and memory ability of VD rats through mechanisms related to anti-apoptosis. CONCLUSIONS: The capacity for ginsenoside Rg2 to modulate the expression of apoptotic related proteins suggests that ginsenoside Rg2 may represent a potential treatment strategy for vascular dementia or other ischemic insults.

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RGD ID: 2290557
Created: 2008-03-19
Species: All species
Last Modified: 2008-03-19
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.