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

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.

SUBMITTER: Yan X

PROVIDER: S-EPMC5552808 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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

Yan Xue X Li Yanfei Y Yu Han H Wang Wei W Wu Chunyan C Yang Yang Y Hu Yongjia Y Shi Xiujuan X Li Jue J

Scientific reports 20170810 1

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 w ...[more]

PMID: 28798484

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Project description:BackgroundEpigallocatechin gallate (EGCG) is a polyhydroxy phenolic compound extracted from tea and its antitumor effect has received widespread attention. We explored the inhibitory effect of EGCG on dimethylhydrazine (DMH)-induced colorectal cancer (CRC) using a rat model, predicted the interaction between EGCG and CRC target genes using a database, and explained the EGCG associated target pathways and mechanisms in CRC.AimTo understand the inhibitory mechanisms of EGCG on CRC cell proliferation and identify its pharmacological targets by network pharmacology analysis.MethodsDMH (40 mg/kg, s.c., twice weekly for eight weeks) was used to induce CRC in rats. After model establishment, the rats were administered with EGCG (50, 100, or 200 mg/kg, p.o., once daily for eight weeks) and killed 12 and 20 wk after the start of the experiment. Formation of aberrant crypt foci and tumor was studied by histological analysis. Using network pharmacology analysis, candidate and collective targets of EGCG and CRC were identified, and Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were used to predict the pathways altered by EGCG.ResultsAt week 12, high-dose EGCG treatment significantly reduced the tumor formation rate, total number of tumors, cancerous and non-cancerous tumors, tumor volume, ascites formation, and aberrant crypt foci count. At week 20, all three doses of EGCG were effective. Seventy-eight collective targets of EGCG and CRC were identified, of which 28 genes were dysregulated in CRC. Kyoto Encyclopedia of Genes and Genomes and GO analyses showed that the dysregulated genes were enriched in hsa05210 (CRC), hsa04115 (p53 signaling pathway), and hsa04151 (PI3K-Akt signaling pathway), GO:0043124 (negative regulation of I-kappaB kinase/NF-kappaB signaling pathway), GO:0043409 (negative regulation of mitogen-activated protein kinase cascade), and GO:2001244 (positive regulation of intrinsic apoptotic signaling pathway) respectively.ConclusionEGCG inhibits the formation of DMH-induced CRC by regulating key pathways involved in tumorigenesis.

Dataset Information

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

Publications

Epigallocatechin-3-gallate inhibits H<sub>2</sub>O<sub>2</sub>-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor.

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