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Epigallocatechin-3-gallate (EGCG) is one of the major polyphenolic compounds present in green tea extracts and has been used as a potential drug for the treatment of numerous diseases. Although the anti-oxidative and anti-apoptosis capabilities of EGCG had been previously demonstrated in cardiac and endothelial cells, whether EGCG can also inhibit the apoptosis of vascular smooth muscle cells (VSMCs), as well as its molecular mechanisms remain unknown. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse VSMCs.
VSMCs were separated from abdominal aorta of mice and the subculture cells at passages 3-8 were used in all the experiments. VSMCs were treated with 10μM, 50μM, 100μM, 150μM of EGCG for 2 hours prior to treatment with 200μM H2O2 of 30min.
Treatment with H2O2 significantly decreased the cell viability and induced apoptosis of VSMCs, which were attenuated by pretreatment with EGCG. In particular, EGCG pretreatment significantly inhibited the H2O2-induced upregulation of cleaved forms of caspase-3, caspase-8, and caspase-9, Bax, CathepsinD, and downregulation of Bcl-2. Moreover, the antioxidation effect of EGCG on VSMCs was determined to be associated with the 67kD laminin receptor (67LR).
In summary, our results demonstrated that EGCG improved cell viability and protected VSMCs against oxidative stress through both extrinsic and intrinsic pathways, while 67LR is likely to be an active and key receptor of EGCG. We thus provide a novel molecular mechanism of EGCG in inhibiting H2O2-induced apoptosis in VSMCs, as well as its function in preventing the development of atherosclerosis.