Molecular Mechanism of Astragaloside IV in Improving Endothelial Dysfunction of Cardiovascular Diseases Mediated by Oxidative Stress.
Peipei MengRui YangFenjun JiangJianbo GuoXinyu LuTao YangQingyong HePublished in: Oxidative medicine and cellular longevity (2021)
Endothelial dysfunction, induced by oxidative stress, is an essential factor affecting cardiovascular disease. Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis. As a main active ingredient of astragalus, astragaloside IV can reduce the apoptosis of endothelial cells during oxidative stress. This review is aimed at exploring the mechanism of astragaloside IV in improving oxidative stress-mediated endothelial dysfunction relevant to cardiovascular diseases. The findings showed that the astragaloside IV can prevent or reverse the uncoupling of eNOS, increase eNOS and NO, and enhance several activating enzymes to activate the antioxidant system. In-depth validation and quantitative experiments still need to be implemented.
Keyphrases
- nitric oxide synthase
- oxidative stress
- nitric oxide
- cardiovascular disease
- endothelial cells
- dna damage
- reactive oxygen species
- ischemia reperfusion injury
- diabetic rats
- induced apoptosis
- hydrogen peroxide
- cell death
- type diabetes
- optical coherence tomography
- endoplasmic reticulum stress
- coronary artery disease
- high resolution
- heat shock
- high glucose
- cell proliferation
- anti inflammatory
- cardiovascular events
- mass spectrometry