大鼠局灶性脑缺血再灌注后瞬时感受器电位C1、M7的表达变化

Expressions of transient receptor potential canonical 1 and melastafin 7 following focal cerebral ischemia-reperfusion injuries in rats

目的研究大鼠局灶性脑缺血再灌注后瞬时感受器电位（TRP）C1和TRPM7的表达变化，进一步探讨局灶性脑缺血再灌注损伤的分子病理机制。方法将50只Wistar大鼠按照随机数字表法分为假手术组、缺血2h再灌注3h组、缺血2h再灌注12h组、缺血2h再灌注24h组、缺血2h再灌注72h组，每组10只。线栓法建立大鼠大脑中动脉阻塞再灌注模型，应用RT．PCR、Westernblot和免疫组化染色方法分别检测再灌注后不同时相缺血侧皮层TRPCI和TRPM7mRNA和蛋白水平的表达。结果假手术组TRPCI和TRPM7均有均有少量表达。脑缺血2h再灌注3hTRPCI表达开始增加，随再灌注时间的延长表达逐渐增强，至再灌注12h达高峰，然后逐渐减弱，再灌注72h时仍高于假手术组水平，差异均有统计学意义（P〈0．05）。TRPM7表达也随再灌注时间的延长而增加，高峰在再灌注24h。结论TRPCI和TRPM7参与了局灶性脑缺血再灌注损伤的病理过程。

Objective To investigate the expressions of transient receptor potential canonical 1 （TRPC1） and melastatin 7 （TRPM7） in rat brains after focal cerebral ischemia-reperfusion injuries, and discuss the molecular mechanisms of brain damage caused by focal cerebral ischemia-reperfusion. Methods Rat models of cerebral artery occlusion （MCAO） were established by suture method. Fifty adult Wistar rats were randomly divided into sham-operated group （n= 10） and ischemia-reperfusion group （n=40）. The rats were sacrificed 3, 12, 24 and 72 h after MCAO and the ischemia-reperfusion group was assigned to 4 subgroups （n=10） accordingly. The mRNA expressions of TRPC1 and TRPM7 in the ischemic cortex at different phases after repeffusion were examined by RT-PCR and the protein expressions of them were detected by Western blotting and immunohistochemistry staining. Results Low expression level of TRPC1 and TRPM7 in the rat brain was found in the sham-operated group. The expression of TRPC1 began to increase 3 h after reperfusion and gradually increased with the progress of repcrfusion, peaking at 12 h of reperfusion; the expressions of TRPC1 decreased gradually thereafter, but it was still higher 72 h after reperfusion as compared with that in the sham-operated group （P〈0.05）. Except the peaked expression level of TRPM7 was detected 24 h after reperfusion, the expression trends of TRPM7 were similar to those of TRPC1. Conclusion TRPC1 and TRPM7 may involve in the pathologic process of focal cerebral ischemia-reperfusion injury.