Objective: To investigate the protected effects and mechanism of ursolic acid (UA) against focal cerebral ischemic-reperfusion injury in rats. Method: Totally 120 Sprague-Dawley (SD) rats were randomly divided into six groups as following:sham operation group

ischemic-reperfusion model group

UA 20

40

80

120 mg·kg-1treated groups

20 expremental animals every group

respectively. The model of focal cerebral ischemic reperfusion was established with Zea-Longa occluding suture in rats. Drugs were given immediately by tail injection when the suture was inserted. And 6 h later

the neurological deficits

ratio of infarct volume

water content of the brain were evaluated. Total antioxidative capacity(T-AOC) and the content of creatine kinase (CK)

lactate dehydrogenase(LDH)

malondialdehyde(MDA) in serum were determined. The activity of superoxide dismutase(SOD)

glutathione peroxidase

(GSH-Px)

catalase(CAT) and the content of MDA in brain tissue were determined

and the histopathological changes were observed by haematoxylin and eosin(HE) staining. Result: Compared with sham operation group

the neurological scores of focal cerebral ischemia-reperfusion model group was significantly decreased (P<0.01);the content of CK

LDH

MDA in serum were significantly increased (P<0.01)

and the level of T-AOC was significantly decreased (P<0.01);the ratio of infarct volume and water content of the brain were significantly increased (P<0.01);the activity of SOD

GSH-Px

CAT in brain tissue were significantly decreased (P<0.01)

the content of MDA was significantly increased (P<0.01);and the histopathological changes of brain tissue was appeared. Compared with focal cerebral ischemia-reperfusion model group

the neurological scores of UA (40

80

120 mg·kg-1) treated groups was significantly decreased (P<0.05

P<0.01)

and the contents of CK

LDH

MDA in serum were also significantly decreased (P<0.05

P<0.01)

while T-AOC was significantly increased (P<0.05

P<0.01). The ratio of infarct volume and brain water content of UA (80

120 mg·kg-1) treated groups were significantly decreased (P<0.05

P<0.01)

and the activity of SOD

GSH-Px

GST in brain tissue of UA (80

120 mg·kg-1) treated groups was significantly increased (P<0.05

P<0.01)

and the histopathological changes of UA treated groups were significantly improved compared with ischemia-reperfusion model group. Conclusion: UA can protect focal cerebral ischemic-reperfusion injury in rats

which may be related with its pharmacological effects of enhanceing the activity of antioxidant enzymes and free radical scavenging capacity.