Abstract
Previously, we found that safrole oxide could trigger vascular endothelial cell (VEC) apoptosis. In this study, to investigate its mechanism to induce apoptosis in VECs, the activities of nitric oxide synthetase and phosphatidylcholine specific phospholipase C, the level of reactive oxygen species and the expressions of Fas, integrin beta4 and P53 were analyzed. The data showed that safrole oxide induced apoptosis by increasing the expressions of Fas, integrin beta4 and P53, and depressing the activity of Ca(2+)-independent phosphatidylcholine-specific phospholipase C and intracellular reactive oxygen species levels in VECs.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Apoptosis*
-
Down-Regulation
-
Endothelial Cells / chemistry
-
Endothelium, Vascular / cytology
-
Endothelium, Vascular / drug effects*
-
Endothelium, Vascular / metabolism
-
Humans
-
Integrin beta4 / analysis
-
Integrin beta4 / metabolism
-
Nitric Oxide Synthase / metabolism
-
Reactive Oxygen Species / metabolism
-
Safrole / analogs & derivatives*
-
Safrole / pharmacology
-
Tumor Suppressor Protein p53 / metabolism
-
Type C Phospholipases / metabolism
-
Up-Regulation
-
fas Receptor / metabolism
Substances
-
Integrin beta4
-
Reactive Oxygen Species
-
Tumor Suppressor Protein p53
-
fas Receptor
-
safrole oxide
-
Nitric Oxide Synthase
-
Type C Phospholipases
-
phosphatidylcholine-specific phospholipase C
-
Safrole