Cyanidin ‐3‐O‐glucoside attenuates endothelial cell dysfunction by modulating miR‐204‐5p/SIRT1‐mediated inflammation and apoptosis

AbstractEndothelial cell (EC) dysfunction is a major symptom associated with the initiation of atherosclerosis (AS). Cyanidin ‐3‐O‐glucoside (C3G) has the potentials to attenuate AS symptoms. In the current study, the mechanism driving the effects of C3G on AS rabbits and injured ECs were explored by focusing on the changes in miR‐204‐5p/SIRT1 axis. AS symptoms were induced in rabbits using high‐fatty diet (HFD) plus b alloon catheter injured method and handled with C3G of two doses. Then the changes in artery wall structure, hemodynamics parameters, blood lipid level, systemic inflammation, and miR‐204‐5p/SIRT1 axis were detected. EC dysfunction was imitated by subjecting human umbilical vein endothelial cell s (HUVECs) to TNF‐α, which was then handled with C3G. The changes in apoptosis, inflammation, and miR‐204‐5p/SIRT1 axis were detected. The results showed that the administrations of C3G improved artery wall structure and hemodynamics parameters, decreased blood lipid levels, and suppressed pr o‐inflammatory cytokine production in HFD rabbits, which was associated with the down‐regulation of miR‐204‐5p and the up‐regulation of SIRT1. In in vitro assays, the treatments of C3G suppressed apoptosis, inhibited inflammation, down‐regulated miR‐204‐5p level, and induced SIRT1 le vel in HUVECs. The overexpression of miR‐204‐5p impaired the protective effects of C3G on the injured HUVECs by increasing cell apoptosis and inflammation. Th...
Source: BioFactors - Category: Biochemistry Authors: Tags: Research Communication Source Type: research