白介素33激活P38-MAPK通路保护心肌缺血再灌注损伤

Interleukin 33 prevents myocardial ischemia and reperfusion injury in rats by activating P38-MAPK pathway

目的:探讨白介素33(IL-33)是否通过调控P38MAPK通路影响心肌缺血再灌(I/R)损伤。方法:应用大鼠心肌I/R模型,将32只成年雄性SD大鼠随机分为4组,对照组、模型组、IL-33组、IL-33+SB230580(P38通路抑制剂)组。检测血清中LDH、CK水平及心肌组织中TNF-α、IL-6、总caspase-3、活化caspase-3、Bcl-2、Bax、磷酸化P38(p-P38)表达。结果 :再灌注4 h后,IL-33可明显降低LDH和CK、TNF-α、IL-6、Bax的表达和caspase-3活化,增加Bcl-2、p-P38表达(均P<0.05);SB230580可以一定程度上减弱IL-33的作用。结论 :IL-33可以通过P38-MAPK通路抑制炎症反应和心肌细胞凋亡保护I/R心肌。

Objective To investigate the protective mechanism of Interleukin 33 （IL-33） in preventing myocardial ischemia and reperfusion injury in rats. Methods A rat model with myocardial I/R with 32the adult male SD rats , which were randomly divided into 4 groups： SO group , I/R group , IL-33 ＋ I/R group , SB230580 ＋ IL-33 ＋ I/R group. The levels of LDH, CK, TNF-α, IL-6, HMGB1, Bcl-2, total caspase-3, cleaved caspase-3 and P-P38 were detected. Results After reperfusion, IL-33 significantly decreased the levels of serum LDH and CK and the expression of TNF-α, IL-6 , cleaved caspase-3 , but significantly increased the expressions of Bcl-2, p-P38 （P 〈 0.05）. SB230580 attenuated the protective role of IL-33 on myocardial I/R in a certain degree. Conclusions IL-33 may prevent myocardial I/R injury via inhibiting inflammation and cardiocyteapoptosis by way of P38 MAPK signaling pathway.