Maresin 1 alleviates myocardial ischemia-reperfusion injury in rats by suppressing inflammation.

Myocardial ischemia-reperfusion injury (MIRI) induces severe inflammatory damage to cardiac tissue, leading to structural impairment and functional decline. Maresin 1 (MaR1) is an anti-inflammatory lipid mediator derived from macrophages that has shown protective effects in various inflammatory conditions. This study investigated the anti-inflammatory properties and underlying mechanisms of MaR1 in the context of MIRI, both in vivo and in vitro. A rat model of MIRI was established, and MaR1 was administered subcutaneously once daily for one week prior to model induction. Cardiac function was monitored intraoperatively, and serum and myocardial tissue samples were collected postoperatively for analysis. Structural alterations, myocardial injury biomarkers, and inflammatory cytokines were evaluated. In vitro experiments using H9c2 rat cardiomyocytes assessed the effects of MaR1 on cell viability and proliferation. MaR1 treatment significantly improved cardiac function impaired by MIRI, preserved myocardial architecture, and reduced serum and tissue levels of creatine kinase, lactate dehydrogenase, cardiac troponin I, and pro-inflammatory cytokines (IL-1β, IL-6, IL-8, MCP1, and TNF-α). In contrast, MaR1 enhanced the expression of the anti-inflammatory cytokine IL-10. In cultured cardiomyocytes, MaR1 promoted viability and proliferation. Collectively, these findings demonstrate that MaR1 confers protection against MIRI by attenuating inflammation, preserving myocardial structure, improving cardiac function, and enhancing cardiomyocyte survival, underscoring its potential as a therapeutic agent for ischemic cardiac injury.