@article{APS6469,
author = {Xiao-mei Bao and Chun-fang Wu and Guo-ping Lu},
title = {Atorvastatin attenuates homocysteine-induced apoptosis in human umbilical vein endothelial cells via inhibiting NADPH oxidase-related oxidative stress-triggered p38MAPK signaling},
journal = {Acta Pharmacologica Sinica},
volume = {30},
number = {10},
year = {2016},
keywords = {},
abstract = {Aim: To examine the effect of atorvastatin on homocysteine (Hcy)-induced reactive oxygen species (ROS) production and apoptosis in human umbilical vein endothelial cells (HUVECs).
Methods: HUVECs were cultured with Hcy (0.1−5 mmol/L) in the presence or absence of atorvastatin (1−100 μmol//L) or various stress signaling inhibitors, including the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (DPI, 10 μmol/L), the p38 mitogen-activated protein kinase (p38 MAPK) inhibitor SB203580 (10 μmol/L) and antioxidants N-acetyl cysteine (NAC, 1 mmol/L). Cell apoptosis was evaluated by Annexin V/propidium iodide staining and flow cytometry. ROS were detected by 2′,7′-dichlorodihydrofluorescein diacetate (H2DCFH-DA). NADPH oxidases were evaluated with lucigenin-enhanced chemiluminescence. Hcy-induced expression of p38MAPK protein was measured by Western blotting analysis.
Results: Atorvastatin inhibited endothelial cell apoptosis induced by 1 mmol/L Hcy in a dose-dependent manner and the maximal inhibitory effect was reached at 100 μmol/L. Atorvastatin (10 μmol/L) significantly suppressed Hcy (1 mmol/L for 30 min) induced ROS accumulation (3.17±0.33 vs 4.34±0.31, P},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/6469}
}