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Sci Rep. 2017 Aug 10;7(1):7774. doi: 10.1038/s41598-017-08301-6.

Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor.

Yan X1,2, Li Y3, Yu H1,2, Wang W1,2, Wu C1,2, Yang Y1,2, Hu Y1,2, Shi X4,5, Li J6,7.

Author information

1
Institute of Clinical Epidemiology and Evidence-based Medicine, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China.
2
Key Laboratory of Arrhythmias of The Ministry of Education of China, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China.
3
School of Medical Technology, Shanghai University of Medicine & Health Sciences, Shanghai, 201318, China.
4
Institute of Clinical Epidemiology and Evidence-based Medicine, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China. xiujuansh@tongji.edu.cn.
5
Key Laboratory of Arrhythmias of The Ministry of Education of China, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China. xiujuansh@tongji.edu.cn.
6
Institute of Clinical Epidemiology and Evidence-based Medicine, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China. jueli@tongji.edu.cn.
7
Key Laboratory of Arrhythmias of The Ministry of Education of China, Tongji University School of Medicine, 1239 Siping Road, Shanghai, 200092, China. jueli@tongji.edu.cn.

Abstract

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. The present study aimed to elucidate the role and mechanism of EGCG in protecting against H2O2-induced apoptosis in mouse vascular smooth muscle cells (VSMCs). VSMCs were pretreated with various concentrations of EGCG for 2 hours prior to treatment with H2O2. 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). 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. These findings 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.

PMID:
28798484
PMCID:
PMC5552808
DOI:
10.1038/s41598-017-08301-6
[Indexed for MEDLINE]
Free PMC Article

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