赣南医学院学报
贛南醫學院學報
공남의학원학보
JOURNAL OF GANNAN MEDICAL COLLEGE
2014年
4期
502-504
,共3页
朱海兵%刘琳%冯李长%余海
硃海兵%劉琳%馮李長%餘海
주해병%류림%풍리장%여해
Kir6. 1%Kir6. 2%脑周细胞%免疫印迹分析
Kir6. 1%Kir6. 2%腦週細胞%免疫印跡分析
Kir6. 1%Kir6. 2%뇌주세포%면역인적분석
Kir6. 1%Kir6. 2%brain pericytes%western blot
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。
目的:探討慢性腦低灌註白質損傷後腦週細胞 Kir6.1、Kir6.2的錶達情況。方法:採用蛋白免疫印跡(Western blot)方法檢測慢性腦低灌註白質損傷模型大鼠腦週細胞 Kir6.1、Kir6.2在不同時間點(術後第7 d、14 d、30 d、60 d)的錶達變化。結果:(1)模型組在不同時間點 Kir6.1蛋白錶達均升高,于30 d 達到高峰,與假手術對照組相比差異有統計學意義(P ﹤0.001);(2)模型組在不同時間點 Kir6.2蛋白錶達與假手術對照組相比差異無統計學意義(P ﹥0.05)。結論:慢性腦低灌註白質損傷後腦週細胞 Kir6.1錶達增彊,這提示 Kir6.1/ K-ATP通道可能參與瞭慢性腦白質損傷的病理生理過程;Kir6.1、Kir6.2的錶達在腦週細胞齣現瞭明顯的異質性。
목적:탐토만성뇌저관주백질손상후뇌주세포 Kir6.1、Kir6.2적표체정황。방법:채용단백면역인적(Western blot)방법검측만성뇌저관주백질손상모형대서뇌주세포 Kir6.1、Kir6.2재불동시간점(술후제7 d、14 d、30 d、60 d)적표체변화。결과:(1)모형조재불동시간점 Kir6.1단백표체균승고,우30 d 체도고봉,여가수술대조조상비차이유통계학의의(P ﹤0.001);(2)모형조재불동시간점 Kir6.2단백표체여가수술대조조상비차이무통계학의의(P ﹥0.05)。결론:만성뇌저관주백질손상후뇌주세포 Kir6.1표체증강,저제시 Kir6.1/ K-ATP통도가능삼여료만성뇌백질손상적병리생리과정;Kir6.1、Kir6.2적표체재뇌주세포출현료명현적이질성。
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.