Resolvin D1 Attenuates Myocardial Infarction in a Rodent Model with the Participation of the HMGB1 Pathway

Purpose Myocardial infarction (MI) is associated with high morbidity and mortality worldwide. This study aimed to explore the roles of resolvin D1 (RvD1), a metabolite of omega-3 polyunsaturated fatty acids, in protection against MI and investigate its influences on high mobility group box 1 protein (HMGB1) and related molecular mechanisms. Methods Three-month-old male Sprague-Dawley rats were divided into five groups: sham, MI, MI+0.02 mu g RvD1, MI+0.1 mu g RvD1, and MI+0.3 mu g RvD1. Vehicle control or different doses of RvD1 were injected into the left ventricle (LV) cavity 5 min before MI induction. During MI induction, myocardial ischemia lasted for 45 min followed by 180 min of reperfusion. After the reperfusion, blood and LV samples were collected for biochemical examination. Results The MI group produced a significant increase in myocardial infarct size, serum cardiac biomarkers (LDH and CK-MB), proinflammatory cytokines (TNF-alpha and IL-6), and MDA levels, and a significant decrease in SOD level compared with the sham group. Moreover, a significant upregulation of gene and protein expressions of HMGB1 and its related TLR4 and NF-kappa B were observed in the MI group when compared with the sham group. Pretreatment of RvD1 ameliorated the biochemical changes caused by MI. Conclusions Our results suggested that RvD1 pretreatment exhibited protective effects against MI through downregulation of HMGB1 and its related TLR4 and NF-kappa B expressions.