Methyl isoeugenol

Methyl isoeugenol is an orally active, blood-brain barrier-permeable isoeugenol-type eugenol analog. Methyl isoeugenol promotes the nuclear translocation of Nrf2, upregulates the expressions of HO-1, NQO1 and SOD, and reduces the expression level of MDA. Methyl isoeugenol decreases the nuclear translocation of NF-κB. Methyl isoeugenol inhibits NLRP3 inflammasome-mediated pyroptosis. Methyl isoeugenol reduces cerebral infarction volume and regulates the M1/M2 phenotypic balance of microglia. Methyl isoeugenol can be used for the research of cerebral ischemia-reperfusion injury^[1]. In Vitro:Methyl isoeugenol (0-100 μM; 23.5 h) inhibits the secretion of proinflammatory cytokines, the expression of proinflammatory mediators, and NLRP3 inflammasome-mediated pyroptosis in BV2 microglia induced by LPS (HY-D1056)-ATP (HY-B2176), with the strongest effect observed at the concentration of 100 μM^[1].
Methyl isoeugenol (25-100 μM; 23.5 h) inhibits LPS-ATP-induced oxidative stress in BV2 microglia, upregulates the Nrf2 antioxidant signaling pathway, and suppresses the nuclear translocation of NF-κB, with the strongest activity observed at the concentration of 100 μM^[1]. In Vivo:Methyl isoeugenol (25-100 mg/kg/day; p.o.; daily; 3 days) protects against cerebral ischemia-reperfusion injury in male SD rats, reducing infarct volume by up to 59.8%, improving neurological deficits, suppressing neuroinflammation and NLRP3 inflammasome-mediated pyroptosis, and activating the Nrf2 antioxidant signaling pathway^[1].