Allicin alleviates coronary atherosclerosis of mice via endothelial nitric oxide synthase(eNOS)/nuclear factor erythroid 2-related factor(Nrf2)/heme oxygenase-1(HO-1) signaling pathway

PurposeEndothelial progenitor cells (EPCs) have been revealed to interventions in atherosclerosis (AS) progressions. Traditional Chinese medicines (TCMs) have been discovered to modulate the functions of EPCs. Herein, effects of allicin on EPCs were explored in coronary atherosclerosis (CAS).MethodsAllicin (5 or 10 mg/kg/d) was used to treat the ApoE-/- mice fed with high-fat diet (HFD. TC, TG, LDL-C, and HDL-C were examined. HE staining was applied for observation of CAS lesions. In vitro, EPCs were induced by ox-LDL and then treated with allicin and an eNOS inhibitor, L-NAME. Thereafter, the cell viability, apoptosis and migration were examined using CCK-8, flow cytometry and Transwell methods. Western blot was applied for evaluating eNOS, Nrf2 and HO-1 protein expression. NO production, MDA content, and SOD activity were also measured.ResultsAllicin inhibited CAS progression, decreased serum levels of TC, TG, and LDL-C but increased HDL-C. Moreover, counts of circulating EPCs, and the protein levels of eNOS, Nrf2 and HO-1 were increased by allicin treatment in mice fed with HFD. Allicin suppressed MDA contents but enhanced SOD activities. In vitro, allicin reversed the impacts of ox-LDL induction in EPCs, facilitating cell mobility and NO production, and decreasing apoptosis. L-NAME treatment reversed effects of allicin.ConclusionAllicin alleviated CAS progressions in mice, modulating the cell apoptosis and migration of EPCs via eNOS/ Nrf2/HO-1 pathway.