Effect of interleukin 33 on inflammation response and autophagy in rats with myocardial ischemia-reperfusion injury

MA Rui-song; LI Yuan-hong; JIANG Hong; HU Xiao-rong; LI Xue-fei

doi:10.3969/j.issn.1002-266X.2015.22.001

Abstract：Objective To investigate the protective effect of interleukin 33 (IL-33) on myocardial ischemia-reperfu-sion ( I/R) injury and the mechanism.Methods Thirty-two rats were randomly divided into 4 groups:the control group (n=10), I/R group (model group, n=10), IL-33 group (n=6) and anti-ST2 group (n=6).In addition to the control group, the left anterior descending coronary artery ligation method was adopted to establish the myocardial I/R injury model in the other groups ( the sham operation group only received anesthesia, open-chest and threading, but not ligation) .Rats in the IL-33+I/R group and anti-ST2+I/R group were separately injected to the caudal vein with 10μg IL-33 and 0.2 mL anti-ST2 (1 mg/mL) 30 min before modeling.After reperfusion for 4 h, we obtained the serum or myocardial tissues to de-tect the following indicators of each group:(1) the serum lactate dehydrogenase (LDH) and creatine kinase (CK) level:using spectrophotometry, (2) Th1 inflammation factors in the myocardial tissues (TNF-α, INF-γand IL-6) and Th2 in-flammatory cytokines (IL-4, IL-5 and IL-3):using the ELISA, (3) the relative expression of autophagy protein LC3 and beclin 1 in the myocardial tissues:using Western blotting.Results (1) LDH and CK level:the model group was signifi-cantly higher than the control group, IL-33 group was significantly lower than the model group (P<0.05), and no statisti-cal difference was found between the anti-ST2 group and the model group.(2) the inflammation factor expression in the myocardial tissues:Th1 type inflammation factor expression: the model group and IL-33 group were significantly higher than the control group, IL-33 was significantly lower than the model group (all P<0.05), and no difference was found be-tween the anti-ST2 group and the model group.Th2 type inflammation factor expression:the model group was significantly lower than the control group, IL-33 group was significantly higher than the model group, and no statistical difference was found between the anti-ST2 group and the model group.(3) The relative expression of autophagy protein LC3 and beclin-1 in the myocardial tissues:the model group was significantly higher, IL-33 group was significantly lower than the control group, IL-33 was significantly lower than the model group ( all P<0.05) , no significant difference was found between the anti-ST2 group and the model group.Statistically significant differences were found in all indexes between the IL-33 and an-ti-ST2 group.Conclusion IL-33 may attenuate myocardial I/R injury by inhibiting the excessive autophagy, weakening Th1 inflammatory response and enhancing Th2 inflammatory response.