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

Abstract

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.

Troxerutin Protects Against Myocardial Ischemia/Reperfusion Injury Via Pi3k/Akt Pathway in Rats

“…5B, troxerutin significantly increased p-Akt in H9c2 cells in a dose- and time-dependent manner. ROS release is thought to be important in the pathogenesis of myocardial I/R injury [27]. Our study found that the treatment of H9c2 cells with troxerutin markedly reduced H 2 O 2 -induced cell death compared to H 2 O 2 treatment alone.…”

Up-Regulation of HMGB1 Exacerbates Renal Ischemia-Reperfusion Injury by Stimulating Inflammatory and Immune Responses through the TLR4 Signaling Pathway in Mice

“…Thus, HMGB1, which serves as a promoter of the inflammatory responses, was recently discovered as pro-inflammatory cytokine [12]. TNF-α and IL-6 are the typical cytokines that could exacerbate IRI, thus it could be concluded that HMGB1 plays a pathogenic role in I/R, as illustrated by the up-regulation of HMGB1 and the generation of inflammatory factors in the kidney after I/R [31]. More importantly, in the I/R and HMGB1 groups, the levels of TNF-α, IL-6, IFN-γ and IL-1β were much lower in the TLR4 -/-mice than those in the WT mice.…”

Circulating miR-181a as a Potential Novel Biomarker for Diagnosis of Acute Myocardial Infarction

“…Oxidative stress may play an etiological role in AMI and be useful as a biomarker [49]. When oxidative stress occurs, cells trigger a series of biochemical cascades to alter the redox balance and restore homeostasis following the development of atherosclerotic plaques and subsequent AMI [49].…”

“…When oxidative stress occurs, cells trigger a series of biochemical cascades to alter the redox balance and restore homeostasis following the development of atherosclerotic plaques and subsequent AMI [49]. During AMI, the miRNAs involved in inflammation may be indicators of the oxidative-stress response that maintains cellular homeostasis under ischemic and hypoxic conditions [50].…”