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Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A‐induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells
Author(s) -
Mohsenzadeh Mahdieh Sadat,
Razavi Bibi Marjan,
Imenshahidi Mohsen,
Mohajeri Seyed Ahmad,
Rameshrad Maryam,
Hosseinzadeh Hossein
Publication year - 2021
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.6861
Subject(s) - umbilical vein , epigallocatechin gallate , viability assay , pharmacology , toxicity , malondialdehyde , phenylephrine , green tea extract , apoptosis , chemistry , biochemistry , oxidative stress , antioxidant , biology , medicine , endocrinology , in vitro , polyphenol , food science , green tea , blood pressure
This study was designed to assess bisphenol A (BPA)‐induced vascular toxicity, the effectiveness of green tea extract and epigallocatechin gallate (EGCG) against BPA toxicity, and possible underlying mechanisms. In isolated rat aorta, contractile and relaxant responses as well as malondialdehyde levels were evaluated. Cell viability and effects on the protein levels of apoptotic (bax, bcl2, and caspase‐3), autophagic (LC3), and cell adhesion molecules were calculated using the MTT method and western blotting in human umbilical vein endothelial cells (HUVECs). BPA increased aorta MDA levels ( p < .0001) and decreased vascular responses to KCl [20 and 40 mM ( p < .0001), 80 mM ( p < .001)], phenylephrine [10 −8 , 10 −6 , and 10 −5 M ( p < .001), 10 −7 and 10 −4 M ( p < .0001)], and acetylcholine [10 −6 M ( p < .01), 10 −5 and 10 −4 M ( p < .0001)]. In HUVECs, BPA enhanced the levels of LC3A/B, bax/bcl2 ratio, cleaved caspase‐3, and vascular cell adhesion molecule‐1. Green tea extract, EGCG, and vitamin E co‐treatment with BPA diminished the toxic effects of BPA. These findings provide evidence that green tea extract and EGCG possess beneficial effects in preventing BPA‐induced vascular toxicity through increasing the antioxidant activities and the regulation of signaling pathways.