ABSTRACT
Coronary heart disease (CHD) is a hypoxia related
disease. However, the relationship of the hypoxia-induced oxidative stress,
autophagy and apoptosis in cardiomyocyte remains unclear. In this study, we used CoCl2 to mimic
hypoxic conditions in H9c2 cardiomyocytes and study the effects of CoCl2-induced hypoxia on oxidative stress, apoptosis and autophagy, as well as the
relationships among these processes. Cell viability and levels of ROS, LC3-II,
p62, caspase-3 and PARP were assessed. The viability and morphology of
cardiomyocytes were affected by hypoxia, and hypoxia
enhanced levels of ROS and the levels of the LC3-II, p62, caspase-3 and PARP
proteins in H9c2 cells in a dose-dependent manner. ROS levels rise gradually in the
presence of hypoxia; however, it shrinks when
hypoxia reaches a certain level. Caspase-3 and PARP levels were raised with the
increasing of hypoxia level. Enhanced level of LC3 and decreased levels of p62
in hypoxic cells indicate that autophagy levels are in accord with hypoxia. Based
on these results, hypoxia induces oxidative stress, apoptosis and autophagy in
cardiomyocytes. Autophagy is a double-edged sword. At a low level, autophagy
can resist oxidative stress and protect cardiomyocytes from oxidative stress, while
high level autophagy can promote apoptosis of cardiomyocytes.
Share and Cite:
Feng, Q. , Shao, Y. , Jiao, R. , Wei, H. , Dai, M. , Xie, H. , Xu, C. and Li, J. (2019) Effects of Hypoxia on Oxidative Stress, Autophagy and Apoptosis in Cardiomyocytes.
Advances in Biological Chemistry,
9, 54-67. doi:
10.4236/abc.2019.92005.