Objective: To investigate the effect of Buyang Huanwu Tang(BYHWT) on the expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN) mRNA and platelet activation in rat models with cerebral ischemia-reperfusion injury. Method: Sixty specific pathogen free (SPF) Sprague-Dawley rats (weighing 250-300 g) were randomly divided into 5 groups as following:sham-operated group

clopidogrel group

high-dose BYHWT group

low-dose BYHWT group

and model group

12 rats in each group. The high-dose BYHWT group and the low-dose BYHWT group were ig administered with 26

6.5 g·kg-1·d-1 BYHWT respectively while the clopidogrel group was ig administered with 6.8 mg·kg-1·d-1. Another two groups were ig administered with normal saline. After treatment of the animals for 14 days

middle cerebral artery occlusion method was used to establish models of transient focal cerebral ischemia and reperfusion

and corresponding ig treatment was provided 2 h before modeling. The plugging wire was removed after modeling for 60 min and reperfusion for 12 h before samples collection for determination of the content of P-selection(CD62P) in plasma and expression of PTEN mRNA in hippocampus. Result: The neurological score in model group was significantly higher than that in sham-operated group

and the neurological scores in various treatment groups were significantly lower than that in model group.The expression of CD62P in the model group was significantly higher than that in sham-operated group (P<0.05). BYHWT groups and clopidogrel group can significantly inhibit the expression of CD62P (P<0.05)

but without significant difference between BYHWT groups and clopidogrel group. PTEN mRNA expression in model group was significantly higher than that in sham-operated group. PTEN mRNA expression in various treatment groups were significantly lower than that in model group (P<0.05)

mostly significant in BYHWT high dose group. Conclusion: The neuroprotective mechanism of BYHWT on acute cerebral ischemia model may relate with down-regulating the expression of PTEN gene over-expression and inhibiting expression of CD62P.