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. At 4 h 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 HMGB1 and IL-17A were detected by Western Blotting and the expression of TNF-α and IL-6 were detected by Elisa. Results:After 4 h reperfusion, compared with the I/R group, IL-23 significantly increased the infarct size, the apoptosis of cardiomyocytes and the levels of LDH and CK (all P<0.05). Meanwhile, IL-23 significantly increased the expression of eIL-17A, TNF-α and IL-6 and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R (all P<0.05). IL-23 had no effect on the expression of HMGB1 (P>0.05). All these effects were abolished by anti-IL-23 administration. Conclusion: The present study suggested that IL-23 may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

R542.2

湖北省自然科学基金面上项目(2015CFB701)