Epigallocatechin inhibits PDGF-BB-induced vascular smooth muscle cells proliferation via DNMT1 regulation of the Nur 77 axis

EGCG inhibits vascular smooth muscle proliferation.Nur77 and DNMT1 have been observd in the plaques of patients with atherosclerosis and are thought to be associated with vascular smooth muscle cell proliferation. This study was designed to investigate the role and mechanism of epigallocatechin gallate (EGCG) on proliferation and migration of vascular smooth muscle cells( VSMCs) and clarified the underlying molecular mechanism of EGCG. We investigated whether EGCG suppressed platelet-derived growth factor(PDGF)-induced vascular smooth muscle cell proliferation, migration and apoptosis in vivo and vitro. The effect of EGCG on smooth muscle cell proliferation and phenotype were evaluated using Cell Counting Kit-8(CCK8), EdU staining, immunohistochemistry and Western blot analysis.The effect of EGCG on smooth muscle cell migration was uising Wound-healing assay and Western blot analysis..The effect of EGCG on smooth muscle cell apoptosis was uising Flow cytometry and Western blot analysis. The current findings demonstrated that EGCG alleviated neointimal hyperplasia in balloon-induced arterial walls in vivo, significantly inhibited PDGF-BB-induced VSMC proliferation, migration, and promoted apoptosis in vitro and identical results were obtained in vivo..Moreover, EGCG attenuated VSMC proliferation by modulating the regulation of the DNMT1-Nur77-signaling axis. Our collective data showed that EGCG inhibited PDGF-BB-induced VSMC proliferation via DNMT1 regulation of the Nur77- signaling axis. In conclusion, These findings suggest that EGCG may be a promising therapeutic agent for the prevention and treatment of CVDs.