慢性脑低灌注白质损伤后脑周细胞Kir6.1、Kir6.2的表达

Expression of Kir6. 1、Kir6. 2 in Afterbrain Pericyte After White Matter Injury Under Chronic Cerebral Hypoperfusion

目的:探讨慢性脑低灌注白质损伤后脑周细胞Kir6.1、Kir6.2的表达情况。方法:采用蛋白免疫印迹(Western blot)方法检测慢性脑低灌注白质损伤模型大鼠脑周细胞Kir6.1、Kir6.2在不同时间点(术后第7 d、14 d、30 d、60 d)的表达变化。结果:(1)模型组在不同时间点Kir6.1蛋白表达均升高,于30 d达到高峰,与假手术对照组相比差异有统计学意义(P<0.001);(2)模型组在不同时间点Kir6.2蛋白表达与假手术对照组相比差异无统计学意义(P>0.05)。结论:慢性脑低灌注白质损伤后脑周细胞Kir6.1表达增强,这提示Kir6.1/K-ATP通道可能参与了慢性脑白质损伤的病理生理过程;Kir6.1、Kir6.2的表达在脑周细胞出现了明显的异质性。

Objective：To investigate the expression of Kir6. 1、Kir6. 2 in the afterbrain pericyte after white matter injury under chronic cerebral hypoperfusion. Methods：The Western Blot method was used to detect the alterations of the Kir 6. 1、Kir6. 2 proteins in different periods of time（in the postoperative 7th,14th,30th,60th days）in the rat brain peri-cytes after white matter injury under chronic cerebral hypoperfusion. Results：（1）The expression of the Kir6. 1 protein in the model group was increased at different time. It was significantly different from that of the sham operation control group（P ﹤ 0. 01）,and reached the peak in the postoperative 30th day;（2）The expression of the Kir6. 2 protein in the model group is not significantly different from that of the sham operation control group at different points of time（P ﹥0. 05）. Conclusion：The expression of Kir6. 1 is enhanced in the afterbrain pericyte after white matter injury under chro-nic cerebral hypoperfusion. Kir6. 1 / K-ATP channel is involved in the pathophysiological process of chronic cerebral white matter injury;and the expressions of Kir6. 1、Kir6. 2 appear obvious heterogeneity in the brain pericytes.