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氯沙坦对血管紧张素II所致血管平滑肌细胞凋亡及凋亡调控基因的影响 被引量:6

Influences of losartan on the apoptosis and apoptosis genes expression caused by angiotensin II in vascular smooth muscle cells
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摘要 目的:探讨氯沙坦(LT)对血管紧张素II(AngII)对血管平滑肌细胞(VSMC)凋亡和凋亡调控基因的影响。方法:采用流式细胞技术测定在AngII不同浓度和不同作用时间下VSMC凋亡率及凋亡调控基因Fas、bcl-2表达的变化和氯沙坦对其的影响。结果:①随着AngII作用浓度的增加,VSMC凋亡率及Fas,bcl-2基因的表达量均增加(2.35±0.56vs19.71±3.03;Fas:1.36±0.32vs14.67±1.39;bcl-2:2.35±0.51vs16.65±1.42,P<0.01);②LT可促进VSMC的凋亡,促进Fas基因的表达,但可抑制bcl-2基因的表达(19.71±3.03vs27.65±2.11,Fas:14.67±1.39vs20.14±1.41;bcl-2:16.65±1.42vs7.17±1.38,P<0.05);③随着AngII作用时间的增加,VSMC凋亡率及Fas、bcl-2基因的表达均增加(1.43±0.21vs18.56±3.68,Fas:1.21±0.32vs8.62±1.54,bcl-2:2.53±0.71vs15.41±1.63,P<0.01);④随着LT作用时间的增加,VSMC凋亡率及Fas基因的表达均增加,对bcl-2基因的表达则有抑制作用(18.56±3.68vs31.25±2.89,Fas:8.62±1.54vs17.46±1.47;bcl-2:15.41±1.63vs8.45±1.51,P<0.05)。结论:AngII具有促进VSMC凋亡和凋亡调控基因表达作用;氯沙坦可调节AngII对血管平滑肌细胞的作用。 Objective: To study the influences of losartan on the effects of apoptosis and apoptosis genes expression caused by angiotensin II (AngII) in vascular smooth muscle cells. Methods: Flow cytometer was used to measure the apoptosis rate and the expression of apoptosis genes (Fas and bcl-2) induced by AngII in different concentrations and different action time, and the influence by losartan. Results: (1)with the increasing concentration of AngII, the apoptosis rate and the expression of Fas were increased and reach the highest at a 10-5mol/L-concentration(19.71±3.03; 14.67±1.39), and the expression of bcl-2 peaked at a 10-6mol/L-concentration(16.65±1.42); (2)losartan promoted the apoptosis of VSMC and the expression of Fas, especially at a 10-5mol/L-concentration(27.65±2.11; 14.67±1.39, 20.14±1.41), while it inhibited the expression of bcl-2(16.65±1.42, 7.17±1.38); (3)the apoptsis rate and the expression of Fas and bcl-2 were increased with the prolonged action time of AngII, and they ranked the highest at 18 and 6 hours, respectively(1.43±0.21, 18.56±3.68; 1.21±0.32, 8.62±1.54;2.53±0.71, 15.41±1.63 P<0.01); (4) with the increasing of action time of losartan, the apoptosis of VSMC and the expression of Fas were increased and peaked at 18 and 6 hours, respectively (18.56±3.68, 31.25±2.89;8.62±1.54, 17.46±1.47 P<0.05), while the expression of bcl-2 was inhibited and was significantly at 18 hours(15.41±1.63, 8.45±1.51 P<0.05).Conclusions: The apoptosis ratio and the expression of apoptosis genes may be induced and increased by AngII with the increase of the concentrations and the action time. Losartan may have the regulating effect on the apoptosis rate and the expression of apoptosis genes in vascular smooth muscle cells.
出处 《山东大学学报(医学版)》 CAS 北大核心 2005年第6期492-495,共4页 Journal of Shandong University:Health Sciences
基金 2003年山东省科技攻关计划项目(编号:032050114)
关键词 血管紧张素Ⅱ 平滑 血管 细胞凋亡 基因 Fas 基因 BCL-2 氯沙坦 Angiotensin II Muscle, smooth, vascular Gene, Fas Gene, bcl-2 Losartan
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