Objective: To observe the protective effect of baicalin on cerebral ischemia/reperfusion in rats. Method: Fifty adult Sprague-Dawley rats were randomly divided into five groups as following:sham group

model group

135 mg·kg-1 baicalin group

45 mg·kg-1 baicalin group

15 mg·kg-1 baicalin group

with 10 in each group. The sham and model groups received distilled water ig at the same volume and time points as the baicalin groups. Drug or distilled water was administered once a day for 7 d. One hour later after the last administration with baicalin

the middle cerebral artery occlusion was adopted to establish the focal cerebral ischemia/reperfusion model. After 24 h of ischemia/reperfusion

the neurological deficit scores were evaluated. Histopathology changes were observed by hematoxylin and easin(HE) and TdT-mediated dUTP nick end labeling(TUNEL) staining. The levels of superoxide dismutase(SOD)

malondialdehyde(MDA)

tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in cerebral tissue were measured by commercial kit. Result: Compared with the sham group

the model group showed severe pathomorphological damages

significantly higher neurological deficit scores and neural apoptosis

MDA

TNF-α and IL-1β(P<0.01)

but remarkably inactive(P<0.01). Compared with the model group

baicalin could improve the histopathology injury

decrease neural apoptosis

baicalin high dose group significantly decreased neurological deficit scores(P<0.01)

baicalin middle and high dose groups significantly increased the activities of SOD(P<0.05) and decreased the levels of MDA

TNF-α and IL-1β(P<0.01). Baicalin low dose group also significantly decreased the levels of IL-1β(P<0.01). Conclusion: The baicalin had the cerebral protective effect on cerebral ischemia/reperfusion rats

the mechanism may be related to its characteristics of anti-apoptosis

reduction of free radical damage and suppression of inflammation.