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.
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