| Alzheimer's Disease (AD) is characterized by the presence of extra cellular senile plaques (SPs) and intracellular neurofibrillary tangles (NFT) in the brain. The major protein component of SPs is beta Amyloid peptide (Aβ).Aim:We investigated the involvement of HSP70 and N-methy-D-asparagic acid receptor (NMDAR) in the metabolism of the P-amyloid precursor protein and Rg2 influence its derivativeβ-amyloid 1-40 in cultured rat hippocampal neurons, which was injured by ischemical reperfusion through oxygen and glucose deprivation (OGD).Mathods:A Methyl thiazolyl tetrazolium (MTT) assay were used to assess cellular viability, immunocytochemical techniques and Western blot analysis were used to assess the expression of HSP70, NMDA, Aβ1-40 and APP.Results:The data showed that the viability of neurons was decreased after ischemical reperfusion injury. The expression of APP, HSP70, NMDA andβ-amyloid 1-40 was increased after ischemic reperfusion injury and decreased after treatment with ginsenoside Rg2 except HSP70, which increased.Conclusion: These results demonstrate that ginsenoside Rg2 plays a protective role in hippocampal neurons from OGD-induced injury and suggest that this protective effect involves modulation of NMDA receptors and calcium influx.,otherwise, HSP70,which contribute to the fold of beta Amyloid peptide.
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