Objective To observe the neuroprotective effect of atorvastatin and its influence to tumor necrosis factor-alpha(TNF-α) and intedeukin-10(IL-10)in intraeerebral hemorrhage(ICH)rats,and to explore the possible mechanism of its neuroproteetive effect.Methods ICH WaS induced by stereotaxic infusion of collagenase into the right baSal ganglia,the expressions of TNF-α,IL-10 in the serum and brain tissue were analyzed by enzyme linked immunosorbent assay(ELISA),HE staining was used to evaluate the number of activated microglia.Results (1)The numbers of activated mieroglia,TNF-α and IL-10 were have significant differences between group A and group B(all P＜0.05).(2)In comparision with group B,numbers of activated mieroglia in group C,D and E were significantly redueed(P＜0.05).Atorvastatin cause a dose-dependent regulation,which decreased the level of TNF-α and inereased the level of IL-10 significantly(all P＜0.05).Conclusion The down-regulation of TNF-α and up-regulation of IL-10 might partly attribute to the neuropmtection of atovastatin.

Objective To observe the effect of polydatin on nerve cell apoptosis and the influence of the caspase-8 and FLIP protein expression after ischemia reperfusion injury. Methods Thirty rats were randomly divided into sham operation group, model group and polydatin group. The middle cerebral artery occlusion (MCAO) model of focal cerebral ischemia was established by the method of thread embolism. Rats were subjected to adaptive feeding for the first 7 days and then recieved the treatment for another 10 days. The model of ischemia reperfusion injury was established at the 14th day. The polydatin group received 15 mg/kg of polydatin, and the sham operation group and the model group with the same volume of saline once a day for 15 days. The expression of caspase-8 and FLIP protein in the hippocampus of rats were observed by immunohistochemical staining. The expression of caspase-8 and FLIP protein in the hippocampus of rats were observed by TUNEL method at 72 h after cerebral ischemia-reperfusion. Results Compared with the model group, the number of apoptotic cells of polydatin group significantly decreased in hippocampus CA1 region (P<0.01); The expression of caspase-8 (148.78 ± 6.82 vs. 89.61 ± 7.76) in the polydatin group significantly decreased and the expression of FLIP (127.60 ± 8.52 vs. 150.22 ± 8.53) in the polydatin group was increased significantly in hippocampus CA1 region(P<0.01). Conclusions Polydatin have a protection effect on ischemia reperfusion injury in rats and its mechanism may be inhibition of caspase-8 protein expression, promote the FLIP protein expression.