Abstract: AIM: To investigate the protective mechanism of acanthopanax senticosus injection (ASI) on focal cerebral ischemia injury in rats.METHODS: Wistar rats were randomly divided into sham operated group, model control group and two ASI groups, to which ASI of 45 and 90 mg/kg was intraperitoneally administered for 7d, and then subjected to cerebral ischemia injury induced by middle cerebral artery occlusion (MCAO) in rats, via string ligation of arteria carotis interna.The content of maleic dialdehyde (MDA) was determined by thibabituric acid (TBA) test and the activity of superoxide dismutase (SOD) was detected by chemical colorimetry test in cerebral tissues.Apoptosis in cortex region was measured with TUNEL method.Bcl-2, bax and caspase-3 protein expression of neurons was detected with immunohistochemistry staining in cortex region.RESULTS: ASI (45, 90 mg/kg) could significantly decrease the content of MDA and increase the activity of SOD, and inhibit the neuronal apoptosis.ASI (45, 90 mg/kg) could increase the expression of bcl-2 protein, and reduce the expression of bax and caspase-3 protein significantly.CONCLUSION: The protective mechanism of ASI on focal cerebral ischemia injury may be related to anti-free radical effect and inhibition of neuron apoptosis.

Key words: acanthopanax senticosus injection, cerebral ischemia, free radical, apoptosis