目的观察缺血后处理对脑缺血再灌注后缝隙连接蛋白43(Cx43)的影响。方法 30只Wistar雄性大鼠随机分为假手术(Sham)组、缺血再灌注(I/R)组、缺血后处理(IP)组。采用线栓法建立大鼠大脑中动脉缺血模型,脑缺血2h后,I/R组予再灌注,IP组给予大脑中动脉血流再通30s,之后阻断血流30s,如此进行3个循环之后予永久再灌注。于脑缺血再灌注后24h行TTC染色观察脑梗死体积、神经功能缺损评分,应用激光共聚焦显微镜观察Cx43蛋白表达量及分布的变化,行各组间比较。结果 IP组脑梗死体积明显小于I/R组,IP组神经缺损评分低于I/R组,与Sham组相比,I/R组Cx43数量明显减低、分布紊乱,IP组Cx43表达数量及分布明显好于I/R组。结论缺血后处理可减小脑梗死体积、减轻神经功能缺损,缺血后处理能抑制Cx43表达减少、改善Cx43分布情况。
Objective To investigate the effects of ischemic postconditioning on connexin 43 after ischemia/reperfusion.Methods Thirty adult male Wistar rats were randomly divided into Sham group,ischemia/reperfusion(I/R) group,and ischemic postconditioning(IP) group.Models were induced by focal ischemia for 2 h with middle cerebral artery occlusion(MCAO) and 24h reperfusion.Rats in IP group were treated with postconditioning after 120 min of occlusion.Twenty-four hours after reperfusion,neurological scores of rats were measured.Then the rats were killed and the brains were stained by 2,3,5-triphenyltetrazolium chloride(TTC) to measure the size of infarct.We used confocal scanning laser microscope to observe the distribution and expression of Cx43,and compared the differences among groups.Results In IP group,sizes of infarct were extremely smaller than that in I/R group,and neurological scores were lower than that in I/R group.The expression of Cx43 was lower,and with disordered distribution in I/R group.While in IP group,we observed better expression and distribution of Cx43.Conclusion Ischemic postconditioning could decrease the size of infarcts,and preserve the neurological function after ischemia/reperfusion.Ischemic postconditioning could protect Cx43 from I/R injury,which increase the expression of Cx43 and improve the distribution of Cx43.