Abstract: OBJECTIVE: To investigate the protective efficacy of Bunao Fuyuan decoction(BNFY) on cerebral Ischemia/reperfusion(I/R) injury.METHODS: The mouse PC12 cells were chosen,and the oxidative-glucose deprivation/re-oxygenation(OGD/R) injury model were established to simulate cerebral I/R injury. Atorvastatin was selected as a positive drug, and a gradient dose of BNFY was given for 6, 12 and 24 h. 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide(MTT)assay were used to detect cell viability at each time point. Cell apoptosis was measured by terminal deoxynucleotidyl transferase-mediated d UTP-botin nick end labeling(TUNEL) staining. enzyme linked immunosorbent assay was used to detect the expression of tumor necrosis factor(TNF)-α, interleukin(IL)-6, IL-1β and platelet activating factor(PAF).Western blot assay were performed to detect the expression of key regulators [toll-like receptor 4(TLR4), nuclear factor kappa-B(NF-κB), p-p38 mito-gen-activated protein kinase(MAPK) and p-Akt(also known as protein kinase B, PKB)] of cell survival and inflammatory response.RESULTS: The results of MTT assay and TUNEL staining assay revealed that BNFY significantly increased cell viability and inhibited cell apoptosis of PC12 cells following OGD/R, respectively. Furthermore,the expression of TNF-α, 1 L-6, 1 L-1β and PAF were decreased after BNFY treatment. And the results of Western blot assay showed that BNFY downregulated TLR4, NF-κB, p-p38 MAPK expression and upregulated p-Akt expression.CONCLUSION: Our findings suggest that BNFY may play a role in protecting OGD/R injured PC12 cells through inhibiting the inflammatory response and cell apoptosis.

Key words: Inflammatory response, Ischemic stroke, PC12, Oxidative-glucose deprivation/re-oxygenation, Bunao Fuyuan decoction