NF-κB在Jak2/STAT3通路增加大鼠心肌缺血再灌注致脑损伤中的作用

Mechanism of NF-κB Bing Mediated by Jak2/STAT3 Pathway in Brain Injury Induced by Myocardial Ischemia Reperfusion

目的探讨NF-κB在Jak2/STAT3通路增加大鼠心肌缺血再灌注致脑损伤中的作用机制。方法雄性SD大鼠随机分为3组(n=8):假手术组(Sham)、心肌缺血/再灌注组(MIR)、心肌缺血/再灌注+AG490组(MIR+AG)。结扎大鼠冠状动脉左前降支30min再灌注120min建立心肌缺血/再灌注模型。取大鼠脑组织HE染色观察大鼠病理学结果,Western blot法检测凋亡相关蛋白及Jak2、STAT3的表达,Western blot法检测核蛋白中NF-κB/p65的含量。结果与Sham组比较,MIR组脑组织凋亡水平增加:Bax及Cytc表达增多,Bcl-2表达降低;p-Jak2、p-STAT3表达较高,脑组织核蛋白中p65含量增多,反映NF-κB活性增高(P<0.05);与MIR组比较,MIR+AG组脑组织的凋亡水平降低:Bax及Cytc表达减少,Bcl-2表达升高;pJak2、p-STAT3表达减少,NF-κB活性降低(P<0.05)。结论抑制Jak2/STAT3通路可下调NF-κB活性并对心肌缺血再灌注起到保护作用。则Jak2/STAT3通路可能通过活化NF-κB增加脑组织凋亡水平。

Objective To study the mechanism of NF-κB bing mediated by Jak2/STAT3 pathway in brain injury induced by myocardial ischemia reperfusion（MIR）. Methods Male Sprague-Dawley rats were randomly divided into 3 groups （n=8）：Sham group, MIR group, MIR＋AG group. MIR was induced by occlusion of anterior descending branch of left coronary artery for 30min and reperfusion for 120min. The rats were sacrificed after reperfusion and the brains were removed for hematoxylin-eosin H＆E using a microscope. NF-κB/p65 activity is detected by Western blot, as well as apoptosis-related protein and Jak2,STAT3. Results Compared with group sham, Bax, Cytc, p-Jak2, p-STAT3, activity of NF-κB were increased, Bcl-2 was decreased in group MIR （P〈0.05）. Compared with MIR group, Bax, Cytc, p-Jak2, p-STAT3, activity of NF-κB were decreased, Bcl-2 was increased in MIR＋AG group（P〈0.05）. Conclusion Chances are that NF-κB is an important midst link in the mechanism of Jak2/STAT3 pathway aggravating brain injury induced by myocardial IR.