Objective: To investigate the protective effects of Fangji Huangqi Tang(FJHQT) on ischemia-reperfusion(IR) cerebral injury in rats and provide experimental evidence for clinical application of FJHQT on cerebral ischemia. Method: The ischemia-reperfusion model was reproduced by cerebral middle artery occulation for one day. The model rats were randomly allotted into five groups as following:FJHQT 20

40 mg·kg-1

model

sham and positive drug group nimodipine in accordance with the neurobehavioral scores qualified. After being administered orally FJHQT (crude drug

1

2 g·kg-1) or nimodipine (2 mg·kg-1) for continuous 7 days

the cerebral infarct size was observed

and cerebral Na+-K+-adenosine triphosphate(Na+-K+-ATP)

peduced glutathione(GSH)

catalase(CAT) activity and inflammatory cytokines interleukin-6(IL-6)

interleukin-1β(IL-1β)

and tumor necrosis factor α(TNF-α) levels were measured. terminal dUTP nick end labaling(TUNEL) assay was used to determine apoptotic cells in brain tissue. In addition

immunohistochemistry and Western blot analysis were used to determine the expression of Caspase-3. Result: Compared with the sham group

the activities of Na+-K+-ATP

GSH

CAT were decreased in brain tissue of model rats (P<0.01). while inflammatory cytokines IL-6

IL-1β and TNF-α were increased (P<0.01); furthermore

apoptosis level was significantly increased

and the expression of apoptosis protein Caspase-3 also was significantly increased (P<0.01). Compared with the model group

FJHQT could increase Na+-K+-ATP

GSH

CAT activity(P<0.05

P<0.01)

and reduce IL-6

IL-1β and TNF-α levels (P<0.05

P<0.01). FJHQT significantly reduced the degree of apoptosis in brain tissue

as well as Caspase-3 expression (P<0.05

P<0.01). Conclusion: FJHQT can significantly protect against the cerebral ischemia

involving in reduce infarction area of ischemic brain

decrease apoptosis

oxidative damage

inflammation.