Objective:To investigate the protective effects of sodium tanshinone B(STB) on brain damage following focal ischemia-reperfusion(l/R) injury through interfering with N-methyl-D-aspartic acid receptor(NMDAR) and excitatory and inhibitory amino acids,and evaluate the potential mechanisms of the neuroprotective activity of STB.Methods:Transient forebrain ischemia was induced by middle cerebral artery occlusion(MCAO).The rats were randomized into a sham operated group,a model group(l/R) and three STB different dose groups.Rats were pretreated with STB at the doses of 4,8,16 mg/kg(STB_1,STB_2,STB_3) for 3 days before MCAO.The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and y -aminobutyric acid(GABA) were analyzed using high performance liquid chromatography.Results:STB treatment reduced neurological defect scores,cerebral infarction volume and brain water content.The levels of NMDAR1 were significantly higher in the l/R and STB,groups than that of the sham and the STB_3 groups(P<0.01).Optical density of NMDAR1 was significantly increased in cornu ammonis(CA)1 region of the l/R group(P<0.05).STB treatment reduced NMDAR1 optical density in the CA1 region(P<0.01).The levels of glutamate were significantly lower in the hippocampus in the STB_3 group than that of the l/R,STB,and STB_2 groups(P<0.01).Conclusion:Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l/R injury and has potential for future clinical application. Objective: To investigate the protective effects of sodium tanshinone B (STB) on brain damage following focal ischemia-reperfusion (1 / R) injury through interfering with N-methyl-D-aspartic acid receptor (NMDAR) and excitatory and inhibitory amino acids, and evaluate the potential mechanisms of the neuroprotective activity of STB.Methods: Transient forebrain ischemia was induced by middle cerebral artery occlusion (MCAO). The rats were randomized into a sham operated group, a model group (l / R) and three STB different dose concentrations. Rats were pretreated with STB at the doses of 4, 8, 16 mg / kg (STB_1, STB_2, STB_3) for 3 days before MCAO.The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and Results: STB treatment reduced neurological defect scores, cerebral infarction volume and brain water content. These levels of NMDAR1 were significantly higher in the l / R and STB, groups than that of the sham and the STB_3 groups (P <0.01). Optical density of NMDAR1 was significantly increased in cornu ammonis (CA) 1 region of the l / R group density in the CA1 region (P <0.01) .The levels of glutamate were significantly lower in the hippocampus in the STB_3 group than that of the l / R, STB, and STB_2 groups (P <0.01) .Conclusion: Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l / R injury and has potential for future clinical application.