Interleukin 32 participates in cardiomyocyte‑induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
- Yuanyuan Li
- Zhongyan Wang
Affiliations: Department of Cardiovascular Surgery, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China, Department of Geriatrics, The Second Hospital of Tianjin Medical University, Tianjin 300211, P.R. China
- Published online on: July 12, 2022 https://doi.org/10.3892/etm.2022.11504
Copyright: © Li
et al. This is an open access article distributed under the
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Although reperfusion of the ischemic myocardium has been used as a vital treatment of various patients with cardiovascular disease, the accompanying myocardial ischemia‑reperfusion injury (MIRI) can cause further damage, resulting in a poor prognosis. The present study aimed to explore the roles and regulatory mechanisms of interleukin (IL)‑32, a pro‑inflammatory cytokine, in MIRI. Cardiomyocytes were subjected to hypoxia and reoxygenation (H/R) to mimic MIRI. The effects of IL‑32 on oxidative stress, inflammation and apoptosis of H/R‑treated cells were assessed. Given that the nucleotide‑binding oligomerization domain 2 (NOD2) and NADPH oxidase 2 (NOX2) play roles in the inflammatory response and myocardial ischemia, the role of this regulatory axis in the function of IL‑32 was evaluated. The results indicated that IL‑32 levels were elevated following H/R treatment. Downregulation of IL‑32 expression attenuated H/R‑induced reduction in cell viability, LDH release, oxidative stress, inflammation and apoptosis. Moreover, downregulation of IL‑32 expression reversed the activation of the NOD2/NOX2/MAPK signaling pathway caused by H/R treatment. NOD2 overexpression altered the effects of the downregulation of IL‑32 expression on the cells, indicating that this regulatory axis mediated the function of IL‑32. Collectively, the data indicated that IL‑32 participated in the induction of oxidative stress, inflammation, and apoptosis in cardiomyocytes during H/R treatment via the NOD2/NOX2/MAPK signaling pathway.