Propofol attenuates hydrogenperoxide-induced apoptosis in human umbilical vein endothelial cells via multiple signaling pathways.
10.4097/kjae.2015.68.5.488
- Author:
Cheng Lan XIE
1
;
Yin Bing PAN
;
Liu Qing HU
;
Yan Ning QIAN
Author Information
1. Department of Anesthesiology, the First Affiliated Hospital, Nanjing Medical University, Nanjing, China. yanning_qian@sina.com
- Publication Type:Original Article
- Keywords:
Apoptosis;
Human umbilical vein endothelial cell;
Hydrogen peroxide;
Propofol
- MeSH:
Apoptosis*;
Blotting, Western;
Caspase 3;
Cell Count;
Cell Survival;
Endothelial Cells;
Flow Cytometry;
Human Umbilical Vein Endothelial Cells*;
Humans*;
Hydrogen Peroxide;
Oxidative Stress;
p38 Mitogen-Activated Protein Kinases;
Phosphorylation;
Phosphotransferases;
Propofol*;
Protein Kinases
- From:Korean Journal of Anesthesiology
2015;68(5):488-495
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Propofol has been reported to protect vascular endothelial cells against oxidative stress. In this study we investigated its effect on hydrogen peroxide (H2O2)-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and examined the possible signaling pathways. METHODS: HUVECs were pretreated with propofol (1, 5, 25, and 50 microM) for 30 min and then co-incubated with 0.4 mM H2O2 for 4 h. Cell viability was assessed using a Cell Counting Kit-8. Cell apoptosis was analyzed using flow cytometry with annexin V/propidium iodide staining, and evaluated by quantifying caspase-3, Bax, and Bcl-2 expression levels. The expression levels of p38 mitogen activated protein kinase (MAPK), phosphorylated (p)-p38 MAPK, cJun-N-terminal kinases (JNK), phosphorylated (p)-JNK, Akt and phosphorylated Akt [(p)-Akt] (Ser473) were measured by western blotting. RESULTS: H2O2 treatment induced the activation of caspase-3, downregulated Bcl-2 expression, and up-regulated Bax expression, all of which were dose-dependently attenuated by propofol pretreatment. Furthermore, propofol significantly ameliorated H2O2-induced phosphorylation of p38 MAPK, JNK, and Akt in HUVECs. CONCLUSIONS: Propofol can protect HUVECs against H2O2-induced apoptosis via a mechanism that may involve p38 MAPK, JNK, and Akt signaling pathways.
