p38丝裂原活化蛋白激酶在大鼠视网膜缺血再灌注损伤后的磷酸化及其意义  

Phosphorylation of p38-MAPK in rat retina after ischemia- reperfusion injury and its significance

作　　者：许玉花 刘燕[2] 张金玲 

机构地区：[1]通化市眼科医院,吉林通化134001 [2]第四军医大学唐都医院眼科,陕西西安710038 [3]抚松县第二人民医院眼科,吉林白山134504

出　　处：《第四军医大学学报》2007年第8期692-694,共3页Journal of the Fourth Military Medical University

摘　　要：目的:观探讨大鼠视网膜缺血再灌注损伤后p38丝裂原活化蛋白激酶(p38 MAPK)的磷酸化及其意义.方法:采用升高眼内压的方法,制作实验性视网膜缺血再灌注大鼠模型.将30只Wistar大鼠随机分为正常组(n=6)和缺血再灌注组(n=24),其中缺血再灌注组又分为再灌注后2,12,24,72h等4个时间段(每时间段6只).应用Western Blot法检测视网膜组织中p38 MAPK及磷酸化p38 MAPK(p-p38MAPK)蛋白的表达变化.结果:p38 MAPK在缺血再灌注组各时间点的视网膜组织内的表达保持相对恒定,与正常对照组相比无统计学上的变化(P>0.05).p-p38 MAPK的表达水平在缺血再灌注组12h时即有明显升高,24h时达到高峰,72h时仍维持较高的表达水平,与正常对照组相比有统计学著差异(P<0.01).结论:p38 MAPK信号通路的激活可能与缺血再灌注所造成的视网膜损伤有密切关系.AIM： To explore the temporal changes of p38 mitogen-activated protein kinase （MAPK） and its phosphorylation status in rat retina after ischemia-reperfusion injury and its significance. METHODS ： The rat model of experimental retinal ischemia-reperfusion injury was made by increasing the intraocular pressure. Thirty Wistar rats were divided into normal control （ n = 6） and ischemia-reperfusion injury （n = 24） group. The latter group was subdivided into 2, 12, 24 and 72 h after reperfusion （ n =6/time point）. The expressions of p38 MAPK and phosphorylated p38 MAPK （p-p38 MAPK） proteins in rat retina were detected by Western Blot method. RESULTS： The expression level of p38 MAPK protein in rat retina kept unchanged after ischemiareperfusion. However, the expression of p-p38 MAPK protein increased in the retina 12 h after reperfusion injury, reached the peak at 24 h and remained at a higher level at 72 h, which was significantly higher than those in the normal control group （ P 〈 0.01 ）. CONCLUSION： The activation of p38 MAPK signal pathway might play an important role in ischemia-reperfusion-induced retinal injury.

关 键 词：视网膜 再灌注损伤 P38丝裂原活化蛋白激酶类 印迹法 蛋白质 大鼠 

分 类 号：R774.1[医药卫生—眼科]