Aim Reduction of ShengNaoKang decoction (RSNK), is a modified traditional Chinese medicinal formula of ShengNaoKang pill preparation, which is protective in rats against focal cerebral ischemia/reperfusion(I/R) injury.In the current study, we investigate the protective effect of RSNK against apoptosis and oxidative damage induced by cerebral I/R and explore the underlying mechanisms.Cerebral I/R injury was induced by intraluminal middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 24 h in adult male SpragueDawley rats.Rats were randomized into seven groups (n =8) : Sham group, I/R group, RSNKtreated groups(0.7g · kg1, 1.4 g · kg1 and 2.8 g · kg1), nimodipine (NMP)treated group and Whitmania pigra Whitman(WW)treated group.Neurological deficit scores, cerebral humidity content and cerebral infarction volume were measured after the 24 h reperfusion.Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT),inducible nitric oxide synthase (iNOS) and total nitric oxide synthase (TNOS) in serum were measured by assay kits for biochemical analysis.Histological structures of the cortex of the ipsilateral ischemic cerebral hemisphere in rats were observed by Nissl staining.The caspase3 protein content in the hippocampus and cortex was detected by immunohistochemistry.Additionally, Bax and Bcl2 protein expressions in the injured brain were evaluated by Western blot.RSNK administration not only markedly improved neurological deficit scores, but also reduced cerebral humidity content and cerebral infarction volume, lowered MDA content, upregulated SOD and CAT levels,downregulated iNOS and TNOS levels, restrained the expression of caspase3 positive protein and alleviated the Bax and Bcl2 protein expressions.