Inhibitive effects of diethyl-2, 6-diethyl-4-furny- 1,4-dihydropyridine-3, 5-dicarboxylate on the proliferation of vascular smooth muscle cell induced by angiotensin Ⅱ
- VernacularTitle:血管紧张素Ⅱ诱导血管平滑肌细胞增殖过程中呋喃二氢吡啶二羧酸酯的抑制作用
- Author:
Dianxin ZHANG
;
Yusheng REN
;
Lansun LI
;
Hexiang CHENG
;
Bing LIU
;
Haichang WANG
;
Qing ZHANG
;
Rongqing ZHANG
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2005;9(15):212-214
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Vascular smooth muscle cell(VSMC) is one of the major cell components of vascular wall and its pathologic effects in atherosclerosis has been verified and recognized. How to inhibit VSMC proliferation and migration becomes one of the hotspots in the researches regarding the prevention of coronary heart disease(CHD).OBJECTIVE: To observe the impacts of diethyl-2, 6-diethyl-4-furny-1,4-dihydropyridine-3, 5-dicarboxylate(EFDP) on angiotensin Ⅱ (Ang Ⅱ)-induced VSMC proliferation.DESIGN: A randomized controlled study based on VSMC of rabbit' s thoracic aorta cultured in vitro.SETTING: Department of cardiology in a military medical university of Chinese PLA.MATERIALS: The study was conducted in the Laboratory of Cardiology of Xijing Hospital of the Fourth Military Medical University of Chinese PLA between August 2003 and June 2004. Five New Zealand rabbits were selected for the harvest of VSMC. Animal cells were randomly divided into control group, Ang Ⅱ group and Ang Ⅱ + EFDP group(EFDP group).METHODS: New Zealand rabbits were fed by high-fat food. Thoracic aorta was harvested for the separation and culture of VSMC after the injury in thoracic aorta intima by sacculus. The experiment introduced the cultured rabbit VSMC to observe the impacts of EFDP on VSMC DNA synthesis and its time effect during VSMC proliferation promoted by Ang Ⅱ by 3H-TdR method.MAIN OUTCOME MEASURES: 3H-TdR intensity of radio activity in cells of each group to display the DNA synthesis during VSMC proliferation process.RESULTS: Ang Ⅱ could promote the synthesis of rabbit VSMC DNA, which hit its peak at the 36th hour compared with that of control group(358. 00± 49.01 vs 272.42 ± 54.96, P ＜ 0. 01 ) . EFDP had significant inhibitive effects on Ang Ⅱ-induced VSMC proliferation, which also displayed a significant dose-dependent relationship, i.e. with the elevation of EFDP concentration, its inhibitive rate on VSMC proliferation also gradually increased. At the 36th hour, 78.40 μ mol/L of EFDP had more significant effect than that of 0. 08 μmol/L of EFDP(281.50 ± 15.28 vs 349. 25 ±32.10, P＜ 0. 05).CONCLUSION: EFDP can significantly inhibit Ang Ⅱ-induced rabbit VSMC proliferation with certain dose-effect dependency and time responses,which provides a theoretical gist for the primary rehabilitative prevention of atherosclerosis.
