目的 观察大鼠局灶性脑缺血再灌注后不同时间点细胞因子信号转导抑制因子-3(supressor of cytokine signaling 3,SOCS3)的表达情况及实施亚低温后的变化,进一步探讨亚低温的脑保护作用.方法 线栓法制作大鼠大脑中动脉栓塞局灶性脑缺血再灌注模型,同时给予亚低温治疗.HE染色观察病理形态改变,免疫组化法检测SOCS3的表达,TUNEL法检测凋亡细胞.结果 与假手术组相比,常温缺血组于再灌注3 h后SOCS3的表达开始增强,至24 h达高峰,7 天时仍有表达;亚低温缺血组各时间点表达均明显高于常温缺血组(P＜0.05);常温缺血组凋亡阳性细胞数随再灌注时间的延长而逐渐增多,至72 h达高峰;亚低温缺血组各时间点的表达均明显少于常温缺血组(P＜0.05).结论 脑缺血再灌注损伤后SOCS3的表达增强,亚低温可能通过促进SOCS3的表达发挥缺血后抗神经元凋亡的作用.%Purpose To observe the expression of supressor of cytokine signaling 3 ( SOCS3 ) protein and the change with administration of local mild hypothermia after focal cerebral ischemia, and to further investigate the neuroprotective role of mild hypothermia on ischemia brain injury. Methods Focal cerebral ischemia and reperfusion model was established by an intraluminal filament embolism of the middle cerebral artery. Some of the rats were treated by mild hypothermia. Pathological changes were observed with hematoxylin and eosin staining. The expression of SOCS3 was detected by immunohistochemistry, and the apoptotic cells was detected with TUNEL. Results Compared with the sham-operation group, the expression of SOCS3 increased at 3 hour and reached a peak at 24 hour in normal ischemic group. The expression in the mild hypothermia ischemic group increased more obviously than that in normal ischemic group ( P <0. 05 ). The apoptotic cells increased gradually with the elongation of reperfusion time and reached a peak at 72 hour. The expression in the mild hypothermia ischemic group was less obviously than that in normal ischemic group ( P < 0. 05 ). Conclusions S0CS3 protein is activated after focal cerebral ischemia and reperfusion, and mild hypothermia can partially alleviate the apoptosis of neuron after ischemia/reperfusion by enhancing the expression of S0CS3 protein.
展开▼
