Abstract Title:

Epigallocatechin gallate prevents mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis.

Abstract Source:

Phytomedicine. 2019 Jan 30 ;61:152845. Epub 2019 Jan 30. PMID: 31029907

Abstract Author(s):

Chan Zhang, Ping Liao, Ronggan Liang, Xiaojia Zheng, Jie Jian

Article Affiliation:

Chan Zhang


PURPOSE: This study was designed to investigate whether EGCG prevents cardiac I/R mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis.

METHODS: The H9c2 cardiomyocytes hypoxia/reoxygenation (H/R) model in vitro and myocardial ischemia /reperfusion (I/R) model in vivo were made, with or without EGCG treatment. The levels of I/R-induced creatine kinase-MB (CK-MB) and the release of lactate dehydrogenase (LDH), as well as the adenosine triphosphate (ATP) and cardiac functional impairment were examined. Stablely transfecting miR-30a mimic or inhibitor in H9c2 cardiomyocytes was built. The expression of miR-30a, p53 and related proteins in cells was measured by western blotting and qRT-PCR. Cell viability and apoptosis were examined using CCK-8 assay and flow cytometry. The content of reactive oxygen species (ROS), mitochondrial permeability transition pores (MPTP) opening and mitochondrial transmembrane potential (ΔΨm) in cells was measured by fluorescent probes. The levels of miR-30a and p53, some related proteins expression and apoptosis in the cardiac muscle tissues were determined by quantitative real-time PCR (qRT-PCR), H&E staining, western blotting and TUNEL assays.

RESULTS: We found that EGCG preconditioning significantly decreased the levels of CK-MB and LDH, increased the activity of ATP, reduced the apoptotic rate and partially preserved heart function. Furthermore, EGCG decreased ROS levels, MPTP opening and depolarization of ΔΨm, and improved the activity of post-I/R cardiomyocyte. The beneficial effect of EGCG was associated with restored levels of miR-30a expression in the I/R injury that correspond to p53 mRNA downregulation. The regulatory effect of EGCG was greatly enhanced by miR-30a mimic and suppressed by miR-30a inhibitor. More importantly, EGCG pretreatment inhibited the expression of mitochondrial apoptotic related proteins downstream of the miR-30a/p53 pathway.

CONCLUSION: This study demonstrated that EGCG pretreatment may attenuate mitochondrial impairment and myocardial apoptosis by regulation of miR-30a/p53 axis.

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Sayer Ji
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