Oxidative and endoplasmic reticulum stresses are involved in palmitic acid-induced H9c2 cell apoptosis.

Content Provider	Europe PMC
Author	Yang, Lei Guan, Gaopeng Lei, Lanjie Liu, Jianyun Cao, Lingling Wang, Xiangguo
Copyright Year	2019
Abstract	Palmitic acid (PA) is the most common saturated long-chain fatty acid that causes damage to heart muscle cells. However, the molecular mechanism of PA toxicity in myocardial cells is not fully understood. In the present study, we explored the effects of PA on proliferation and apoptosis of H9c2 cardiomyocytes, and uncovered the signaling pathways involved in PA toxicity. Our study revealed induction of both oxidative and endoplasmic reticulum (ER) stresses and exacerbation of apoptosis in PA-treated H9c2 cells. Inhibition of oxidative stress by N-acetylcysteine (NAC) reduced apoptosis and decreased ER stress in PA-treated H9c2 cells. Moreover, inhibition of ER stress by 4-phenyl butyric acid decreased apoptosis and attenuated oxidative stress. In summary, the present study demonstrated that oxidative stress coordinates with ER stress to play important roles in PA-induced H9c2 cell apoptosis.
Page Count	9
ISSN	01448463
Volume Number	39
PubMed Central reference number	PMC6527925
Issue Number	5
PubMed reference number	31064816
Journal	Bioscience Reports [Biosci. Rep]
e-ISSN	15734935
DOI	10.1042/BSR20190225
Language	English
Publisher	Portland Press Ltd.
Publisher Date	2019-05-21
Access Restriction	Open
Rights License	This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). © 2019 The Author(s).
Subject Keyword	apoptosis endoplasmic reticulum stress H9c2 cells oxidative stress palmitic acid
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology Biochemistry Biophysics