Epigallocatechin Gallate Reduces Homocysteine-Caused Oxidative Damages through Modulation SIRT1/AMPK Pathway in Endothelial Cells

Autor: Yu An Chen, Pei-Ling Hsieh, Chi Wen Li, Hsiu Chung Ou, Pei Ming Chu, Kun Ling Tsai, Peiying Pai, Shu Yih Wu, Hsiu I. Chen, Wan Ching Chou, Shih Hung Chan
Rok vydání: 2020
Předmět:
Hyperhomocysteinemia
Apoptosis
AMP-Activated Protein Kinases
030204 cardiovascular system & hematology
Pharmacology
Epigallocatechin gallate
medicine.disease_cause
complex mixtures
Antioxidants
Catechin
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Sirtuin 1
Human Umbilical Vein Endothelial Cells
medicine
Humans
heterocyclic compounds
Homocysteine
Protein kinase B
Protein Kinase C
chemistry.chemical_classification
Reactive oxygen species
Dose-Response Relationship
Drug
Tea
biology
NADPH Oxidases
food and beverages
AMPK
General Medicine
Oxidative Stress
Complementary and alternative medicine
chemistry
030220 oncology & carcinogenesis
biology.protein
sense organs
Signal transduction
Reactive Oxygen Species
Oxidative stress
Nicotinamide adenine dinucleotide phosphate
Phytotherapy
Signal Transduction
Zdroj: The American Journal of Chinese Medicine. 49:113-129
ISSN: 1793-6853
0192-415X
DOI: 10.1142/s0192415x21500063
Popis: Elevated plasma concentration of total homocysteine is a pathological condition that causes vascular endothelial injury and subsequently leads to the progression of endothelial apoptosis in atherosclerosis. Epigallocatechin gallate (EGCG), a well-known anti-oxidant in green tea, has been reported with benefits on metabolic and cardiovascular diseases. This study aimed to explore that EGCG ameliorates homocysteine-induced endothelial cell apoptosis through enhancing the sirtuin 1 (SIRT1)/AMP-activated protein kinase (AMPK) survival signaling pathway. Human umbilical endothelial cells were treated with homocysteine in the presence or absence of EGCG. We found that EGCG significantly increased the activities of SIRT1 and AMPK. EGCG diminished homocysteine-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation by inhibiting protein kinase C activation as well as reactive oxygen species (ROS) generation and recovered the activity of the endogenous antioxidant enzyme, superoxidase dismutase (SOD). Besides, EGCG also restores homocysteine-mediated dephosphorylation of Akt and decreases endothelial NO synthase (eNOS) expression. Furthermore, EGCG ameliorates homocysteine-activated pro-apoptotic events. The present study shows that EGCG prevents homocysteine-induced endothelial cell apoptosis via enhancing SIRT1/AMPK as well as Akt/eNOS signaling pathways. Results from this study indicated that EGCG might have some benefits for hyperhomocysteinemia.
Databáze: OpenAIRE
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