Carvacrol attenuated myocardial infarction through NLRP3-mediated pyroptosis and mTOR/Nrf2/PPARγ-dependent autophagic signaling.

Myocardial ischemia, also known as myocardial infarction or heart attack, is a significant global health issue and a leading cause of mortality worldwide. The present study focuses on investigating the cardioprotective role of carvacrol on three specific pathways: nuclear factor E2-related factor (Nrf2) / peroxisome proliferator-activated receptor factor (PPARγ)-coupled anti-inflammatory response, inflammasome (NLRP3)-mediated pyroptosis, and mammalian target of rapamycin (mTOR)-dependent autophagic signaling. Male Sprague Dawley rats were divided into three experimental cohorts to determine the best dose for carvacrol (20 mg / kg, 50 mg / kg, and 80 mg/ kg) and the optimum treatment strategy.