Objective:To study the effects of oxymatrine(OMT) on brain-derived neurotrophic factor(BDNF) and its receptor tyrosine kinase(TrkB) in cerebral cortex after focal cerebral ischemia-reperfusion in rats

and explore the neuroprotective mechanism of oxymatrine.Methods:The rat middle cerebral artery occlusion models with filament of focal cerebral ischemia-reperfusion were established.SD male rats were divided randomly into sham group

cerebral ischemia-reperfusion model group

nimodipine(Nim) group and the oxymatrine group.the oxymatrine group was futher divided into three sub-groups which were dealt with the low

middle and high dose of oxymatrine.The neurological scores were used after 2 h ischemia followed by 24 h reperfusion.The expression of BDNF positive neurons

BDNF and TrkB proteins were respectively detected by immunohistochemistry and western blot.Results:Compared with the sham group

the neurological scores decreased

while the expression of BDNF positive neurons

BDNF and its receptor TrkB protein significantly increased in middle and high dose of oxymatrine groups(P<0.05;P<0.01).Conclusion:OMT protects the rats from the ischemia injury following focal cerebral ischemia-reperfusion

the mechanism of which may partly be due to up-regulating the expression of BDNF and TrkB.