胡黄连苷Ⅱ对大鼠脑缺血再灌注损伤Caspas-3表达的影响

目的 探讨胡黄连苷Ⅱ对大鼠脑缺血再灌注损伤脑组织半胱天冬酶-3(Caspase-3)表达的影响.方法 线栓法建立大鼠大脑中动脉闭塞再灌注模型;经尾静脉注射胡黄连苷Ⅱ(10 mg/kg)干预治疗,Bederson's法评价动物神经行为功能,苏木精伊红(HE)染色观察脑组织结构,原位末端标记(TUNEL)法检测神经细胞凋亡,免疫组化和酶联免疫法检测Caspase-3的表达.结果 脑缺血2 h再灌注22 h后,大鼠出现神经行为功能障碍,脑组织Caspase-3表达增强,细胞凋亡数较假手术组明显增多(P＜0.01).胡黄连苷组大鼠Bederson's评分,Caspase-3表达以及细胞凋亡数量较阴性对照组显著降低(P＜0.01).结论 胡黄连苷Ⅱ可能通过下调Caspase-3表达,抑制脑缺血再灌注损伤诱导的细胞凋亡,改善动物的神经行为功能.

The interference of picroside Ⅱ on the expressions of Caspase-3 following cerebral ischemia reperfusion injury in rats

Objective To explore the effect of picrodideⅡ on the expressions of Caspase-3 in brain tissue following cerebral ischemic reperfusion injury in rats. Methods The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in rats. Picrodide Ⅱ (10 mg/kg) was injected from tail vein for treatment. The neurological function was evaluated with Bederson's test. The brain structure was observed by hematoxylin-eosin (HE)stain and the apoptosis were counted by TUNEL immunofiuorescence assay. The expressions of Caspase-3 were detected with immunohistochemical and enzyme linked immunosorbent assay. Results After ischemia for 2 h and reperfusion for 22 h, the rats showed neurological function deficit. The expressions of Caspase-3 and the number of apoptotic cells in brain tissue increased significantly than those in the sham operative group (P＜ 0.01). In picroside, the Bederson's scores, the expressions of Caspase-3 and the number of apoptosis cells were significantly lower than those in the negative control group(P＜0.01).Conclusion Picroside Ⅱ might reduce the expressions of Caspase-3 to inhibit the neuronal apoptosis induced by cerebral ischemia reperfusion injury and improve the neurological function of rats.