Vitamin E inhibits homocysteine-mediated smooth muscle cell proliferation.
- Author:
Tong ZOU
1
;
Nan LIU
;
Shu-de LI
;
Yong-chun SU
;
Yong MAN
;
Di LU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antioxidants; pharmacology; Cell Proliferation; drug effects; Cells, Cultured; Homocysteine; pharmacology; Muscle, Smooth; cytology; drug effects; metabolism; Muscle, Smooth, Vascular; cytology; drug effects; metabolism; Rats; Reactive Oxygen Species; metabolism; Vitamin E; pharmacology; alpha-Tocopherol; pharmacology; beta-Tocopherol; pharmacology
- From: Journal of Southern Medical University 2007;27(6):783-786
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of reactive oxygen species (ROS) and the effect of vitamin E on proliferation of vascular smooth muscle cells (VSMCs) induced by homocysteine.
METHODSDNA synthesis in the VSMCs cells was measured using [3H]-thymidine incorporation assay, and the cell number determined by trypan blue method. The level of ROS in the cells was determined using DCF-DA as the fluorescence probe.
RESULTSHomocysteine promoted VSMC DNA synthesis, proliferation, and ROS production. Cysteine resulted in increased ROS production in VSMCs, but had no significant effect on DNA synthesis and cell proliferation. Catalase significantly inhibited ROS production induced by homocysteine, but did not significantly inhibited homocysteine-mediated proliferation of VSMCs. While alpha-tocopherol and beta-tocopherol both suppressed increased ROS production induced by homocysteine in VSMCs, only alpha-tocopherol significantly inhibited homocysteine-mediated VSMC proliferation.
CONCLUSIONROS is not associated with VSMC proliferation, and vitamin E-induced suppression of VSMC proliferation is probably related to protein kinase C inhibition.