title: Apoptosis and calcification of vascular endothelial cell under hyperhomocysteinemia.
abstract: In recent years, it is found that increase in Hcy level in blood can directly or indirectly cause vascular endothelial cell injury and induce vascular calcification. However, the mechanism of vascular endothelial cell injury and vascular calcification has not been studied thoroughly. This paper carried out experiment for research aiming at discussing the effect and action mechanism of Hhcy on endothelial cells and vascular calcification. Firstly, human umbilical vein endothelial cells (HUVECs) were cultured and then intervened by Hcy of different concentrations (0, 0.01, 0.1, 1.0, 3.0, 5.0 mmol/L) and at different action time (3, 6, 12, 24 h). Then apoptosis rate and reactive oxygen were detected by flow cytometry. At the same time, the model for the culture of rat vascular calcification was set up and induced into Hhcy so as to detect the total plasma Hcy level and judge vascular calcification degree. The results showed that with the increase in Hcy concentration and extension of action period, the apoptosis rate and generation of reactive oxygen of HUVECs all significantly increased, and the differences were all statistically significant (P < 0.01). In animal calcification model, mass of black particle deposition was seen after Von Kossa staining of rat vessels in calcification group. Compared with the control group, the vascular calcium content, alkaline phosphatase activity and osteocalcin content in calcification group all increased (P < 0.01). The content of plasma lipid conjugated olefine from highest to lowest wasas follows: calcification plus homoetheionin, homoetheionin, and calcification group. There was no significant difference between the calcification group and control group. All these findings suggested that Hcy could induce the apoptosis of endothelial cells and its effect degree depended on its concentration and action period; Hhcy could promote the calcification of blood vessels, and its mechanism might relate with the strengthening of lipid peroxidation. The above results leave great benefits on clinical prevention works.
authors.affiliation: Coronary Care Unit, The Nanfang Hospital of Southern Medical University, Guangzhou, China.
authors.forename: Kuaifa
authors.initials: K
authors.lastname: Fang
authors.forename: Zhujun
authors.initials: Z
authors.lastname: Chen
authors.forename: Meng
authors.initials: M
authors.lastname: Liu
authors.forename: Jian
authors.initials: J
authors.lastname: Peng
authors.forename: Pingsheng
authors.initials: P
authors.lastname: Wu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002114:Calcinosis / Q000209:etiology* / Q000503:physiopathology*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000473:pathology*; D005434:Flow Cytometry; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications*; D051381:Rats