ROLE OF CARVACROL IN PROLIFERATIVE CELL SIGNALLING AND ISCHEMIC STROKES: A DETAILED REVIEW
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Carvacrol, tissue repair, cell signalling pathway, ischemia-reperfusionAbstract
Plant-based molecules have played important roles in treatment of human diseases as therapeutic agents since ancient times. Carvacrol [2-methyl-5-isopropyl phenol] is among the most studied of the isoprenoid group of bioactive compounds, and has diverse applications in the pharmaceutical, food, biotechnological industries and others. Discovery of its antimicrobial, anticancer, antispasmodic, immunomodulatory, anti-inflammatory, antioxidant and mitogenic effects, has made it a hot topic of numerous research projects. Molecular mechanisms underlying these various effects are still subjects of ongoing researches and existing literatures are quite few on this subject. This review work sought to study the few existing literatures on the carvacrol-cell signalling pathway relationship in cell survival and death, and the emerging future directions for basic and translational research. Carvacrol is known to activate several cell signalling pathways essential to cell survival and death, such as ERK1/2 MAPK signalling, p38 MAPK signalling and JNK MAPK signalling of the MAPK signalling family, PI3K/AKT signalling, IL6/STAT3 signalling, eNOS signalling, etc. Carvacrol exerts different biological actions to influence up-/down-regulation of key cell cycle proteins expressions such as cyclin D1, cyclin B1; CDK4, CDK6, pRb, etc, were either. Mitochondrial-mediated dose-dependent apoptosis and cytoprotection are a major hallmark of mechanism of carvacrol action.
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