The protective effect of umbelliferone ameliorates myocardial injury following ischemia‑reperfusion in the rat through suppression NLRP3 inflammasome and upregulating the PPAR-γ.

Abstract

The present study investigated whether the protective effect of umbelliferone could regulate myocardial injury following ischemia‑reperfusion and improve mitochondrial respiratory function, thereby relieving myocardial injury following ischemia‑reperfusion in rats. In the present study, the extent of inflammation and oxidative stress were analyzed using ELISA. Western blot analysis was employed to investigate the protein expression levels of the PYD domains‑containing protein3 (NLRP3) inflammasome and peroxisome proliferator‑activated receptor-γ (PPAR‑γ). Compared with the myocardial injury following ischemia‑reperfusion group, umbelliferone significantly prevented myocardial injury, inhibited oxidative stress markers (superoxide dismutase and malondialdehyde), reduced inflammation (tumor necrosis factor‑α and interleukin‑6) and myocardial apoptosis levels (caspase‑3/9 and apoptosis regular B‑cell lymphoma‑2‑associated X protein) in the myocardial injury following ischemia‑reperfusion group of rats. Umbelliferone treatment also suppressed NACHT, LRR and NLRP3 inflammasome activation and induced PPAR‑γ expression. The results of the present study suggested that the protective effect of umbelliferone may ameliorate myocardial injury following ischemia‑reperfusion in the rat through the suppression of the NLRP3 inflammasome and upregulating PPAR‑γ expression.