IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions

• Published in: Cellular physiology and biochemistry Vol. 38; no. 6; pp. 2163 - 2172
• Main Authors: Hu, Xiaorong, Ma, Ruisong, Lu, Jiajia, Zhang, Kai, Xu, Weipan, Jiang, Hong, Da, Yurong
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Cell Physiol Biochem Press GmbH & Co KG 01-01-2016
• Subjects: Animals; Apoptosis; Inflammatory responses; Interleukin-17 - immunology; Interleukin-23; Interleukin-23 - immunology; Interleukin-6 - immunology; Male; Myocardial I/R injury; Myocardial Reperfusion Injury - blood; Myocardial Reperfusion Injury - immunology; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocardium - immunology; Myocardium - pathology; Original Paper; Oxidative Stress; Oxidative stress reaction; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha - immunology; Inflammatory responses; Oxidative stress reaction; Myocardial I/R injury; Interleukin-23
• ISSN: 1015-8987; 1421-9778
• DOI: 10.1159/000445572

Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. 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.