Neuroprotective Effects of Carvacrol in Cerebral Ischemia and Hypoxia

Stroke is a leading cause of morbidity and mortality worldwide, characterized by complex pathological processes including ionic imbalance, oxidative stress, neuroinflammation, and apoptosis. Carvacrol, a naturally occurring monoterpenoid phenol, has gained attention in drug development for its potent antioxidant, anti-inflammatory, anti-apoptotic, and transient receptor potential melastatin 7 (TRPM7)-inhibitory properties. This review summarizes current evidence regarding the neuroprotective effects of carvacrol in various in vitro and in vivo models of cerebral ischemia and hypoxia. Mechanistic insights reveal that carvacrol modulates multiple molecular pathways, mitigates oxidative damage, suppresses neuroinflammation, alleviates neuronal apoptosis, and inhibits TRPM7 channel activity in cerebral ischemia and hypoxia. Finally, the broader applications of carvacrol in various diseases and its translational prospects are discussed, emphasizing the need for further preclinical and clinical studies to facilitate its development into a novel neuroprotective agent and adjunctive drug for stroke therapy.