虎杖苷对脑缺血再灌注大鼠海马凋亡相关蛋白表达的影响

目的 观察虎杖苷对脑缺血再灌注大鼠海马caspase-8、Fas相关死亡域样白细胞介素1β转化酶抑制蛋白(Fas-associated death domain-like IL-1 beta converting enzyme inhibitory protein,FLIP)表达的影响,探讨虎杖苷对脑缺血再灌注损伤的保护机制.方法 将30只大鼠随机分为假手术组、模型组、虎杖苷组,每组10只.适应性喂养后7 d开始给药,虎杖苷组大鼠灌胃虎杖苷溶液15 mg/kg,假手术组、模型组灌胃等体积生理盐水,1次/d.连续给药后7 d,采用线栓法建立大脑中动脉闭塞局灶性脑缺血模型.造模后继续给药3 d.脑缺血再灌注后72 h,采用TUNEL法观察各组大鼠脑组织神经细胞凋亡情况;采用免疫组化染色法观察各组大鼠海马caspase-8、FLIP蛋白表达.结果 缺血再灌注72 h,与模型组比较,虎杖苷组海马CA1区凋亡细胞(23.87±3.14)个比(56.69±9.21)个]减少(P<0.01);caspase-8蛋白平均灰度值为(148.78±6.82)比(89.61±7.76)]表达降低、FLIP蛋白平均灰度值为(127.60±8.52)比(150.22±8.53)]表达增高(P<0.01).结论 虎杖苷可减少脑缺血再灌注大鼠海马神经细胞凋亡,其机制可能与抑制caspase-8蛋白表达,促进FLIP蛋白表达有关.

The effect of polydatin on nerve cell apoptosis in hippocampus after ischemia-reperfusion

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.