Open AccessEnalapril attenuates endoplasmic reticulum stress and mitochondrial injury induced by myocardial infarction via activation of the TAK1/NFAT pathway in mice
Author(s) -
Xing Rong,
Donghui Ge,
Lili Yu,
Lei Li,
Maoping Chu,
Haitao Lv
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.8280
Subject(s) - enalapril , endoplasmic reticulum , apoptosis , nfat , microbiology and biotechnology , oncogene , medicine , tunel assay , apoptosis inducing factor , chemistry , endocrinology , biology , programmed cell death , cell cycle , caspase , calcineurin , angiotensin converting enzyme , biochemistry , blood pressure , transplantation
The present study investigated the effect of enalapril on myocardial infarction (MI) and its mechanism of action in mice. Treatment with enalapril significantly attenuated cellular apoptosis and death. In vivo , enalapril treatment alleviated MI injury, and decreased myocardial apoptosis and the size of the infarct area. This was paralleled by increased Bcl-2 expression, decreased Bax expression, a decreased caspase-3 level, decreased expression of endoplasmic reticulum stress-associated proteins, including activating transcription factor 6 and 78 kDa glucose-regulated protein, and fewer TUNEL-positive cells in the heart. Furthermore, enalapril-treatment increased transforming growth factor-activated kinase 1/nuclear factor of activated T cells 3 signaling, which protected the myocardium.