IL-38 attenuates myocardial ischemia-reperfusion injury by inhibiting macrophage inflammation.
Immun Inflamm Dis
; 11(6): e898, 2023 06.
Article
em En
| MEDLINE
| ID: mdl-37382260
ABSTRACT
BACKGROUND:
Reperfusion therapy is the most effective approach to resolve coronary occlusion, but myocardial injury caused by excessive inflammation during myocardial ischemia-reperfusion will also pose a new threat to health. Our prior study revealed the expression pattern of interleukin-38 (IL-38) in the peripheral blood serum of patients with ischemic cardiomyopathy and the role of IL-38 in acute myocardial infarction in mice. However, its role and potential mechanisms in myocardial ischemia/reperfusion injury (MIRI) remain to be determined. METHODS ANDRESULTS:
The left anterior descending artery of C57BL/6 mice was transiently ligated to induce the MIRI model. We found that MIRI induced the expression of endogenous IL-38, which was mainly produced by locally infiltrating macrophages. Overexpression of IL-38 in C57BL/6 mice attenuated inflammatory injury and decreased myocardial apoptosis after myocardial ischemia-reperfusion. Furthermore, IL-38 inhibited lipopolysaccharide-induced macrophage inflammation in vitro. Cardiomyocytes cocultured with the supernatant of IL-38- and troponin I-treated macrophages showed a lower rate of apoptosis than controls.CONCLUSIONS:
IL-38 attenuates MIRI by inhibiting macrophage inflammation. This inhibitory effect may be partially achieved by inhibiting the activation of NOD-like receptor pyrin domain-related protein 3 inflammasome, resulting in decreased expression of inflammatory factors and reduced cardiomyocyte apoptosis.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão Miocárdica
/
Interleucina-1
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article