IL-23对大鼠心肌缺血再灌注损伤中心肌炎症反应及氧化应激的影响  

Effect of interleukin-23 on inflammation response and oxidative stress in rats with myocardial ischemia reperfusion injury

作　　者：张凯[1] 许卫攀 金道群[1] 陈志强[1] 胡笑容[2] ZHANG Kai;XU Wei-pan;JIN Dao-qun;CHEN Zhi-qiang;HU Xiao-rong(Department of Cardiology, Huangshi Central Hospital of Edong Healthcare Group (Affiliated Hospital of Hubei Polytechnic University), Huangshi 435000, China;Department of Cardiology, People's Hospital of Wuhan University, Wuhan 430060, China)

机构地区：[1]鄂东医疗集团黄石市中心医院心血管内科(湖北理工学院附属医院),湖北黄石435000 [2]武汉大学人民医院心血管内科,湖北武汉430060

出　　处：《海南医学院学报》2017年第19期2601-2604,2608,共5页Journal of Hainan Medical University

基　　金：湖北省自然科学基金面上项目(2015CFB701)~~

摘　　要：目的:探讨IL-23对心肌缺血再灌注(I/R)损伤的影响。方法:SD大鼠随机分为4组:假手术(SO)组、缺血再灌注(I/R)组、缺血再灌注+IL-23因子(I/R+IL-23)组和缺血再灌注+IL-23抗体(I/R+anti-IL-23)组。再灌注4小时后,取血清检测乳酸脱氢酶(LDH)和肌酸激酶(CK)水平,取心室肌组织,应用Elisa试剂盒检测丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平以及超氧化物歧化酶(SOD)活力。Western Bolt法检测大鼠心肌组织中高迁移率组蛋白1(HMGB1)和白介素-17A(IL-17A)的蛋白含量。TTC法检测心肌梗死面积,TUNEL法检测心肌细胞凋亡率。结果:再灌注4小时后,与I/R组相比,I/R+IL-23组心肌梗死面积扩大、心肌细胞凋亡率明显增加,血清LDH、CK以及心肌组织中MDA、TNF-α、IL-6水平和IL-17A蛋白含量明显升高,SOD活力明显降低(P<0.05),而HMGB1蛋白含量无明显变化(P>0.05)。这些变化在I/R+anti-IL-23组则刚好相反。结论:研究结果表明IL-23通过促进炎症反应及氧化应激反应而加重心肌缺血再灌注损伤。Objective:To investigate the effect of interleukin-23(IL-23)on myocardial ischemia-reperfusion(I/R)injury.Methods:Male Sprague-Dawley rats were randomly assigned into sham operated control(SO)group,ischemia and reperfusion(I/R)group,(IL-23+I/R)group and(anti-IL-23+I/R)group.At4h after reperfusion,the serum concentration of lactate dehydrogenase(LDH),creatine kinase(CK)and the tissue MDA concentration and SOD activity were measured.The infarcte size was measured by TTC staining.Apoptosis in heart sections were measured by TUNEL staining.The expression of HMGB1and IL-17A were detected by Western Blotting and the expression of TNF-αand IL-6were detected by Elisa.Results:After4h reperfusion,compared with the I/R group,IL-23significantly increased the infarct size,the apoptosis of cardiomyocytes and the levels of LDH and CK(all P<0.05).Meanwhile,IL-23significantly increased the expression of eIL-17A,TNF-αand IL-6and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R(all P<0.05).IL-23had no effect on the expression of HMGB1(P>0.05).All these effects were abolished by anti-IL-23administration.Conclusion:The present study suggested that IL-23may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

关 键 词：白介素-23 炎症反应 氧化应激 心肌缺血再灌注 

分 类 号：R542.2[医药卫生—心血管疾病]