摘要
目的观察缺氧时血管紧张素Ⅱ(AngⅡ)对血管内皮细胞(VEC)内钙离子浓度的影响,探讨金钠多(银杏叶提取物)对VEC的保护作用。方法建立VEC缺氧损伤模型;实验分为空白对照组、单纯缺氧组、缺氧加金钠多保护组、单纯AngⅡ作用组、AngⅡ加金钠多保护组、缺氧加AngⅡ作用组、缺氧加AngⅡ加金钠多保护组等7组。各组细胞经过Fluo-3/AM负载后,用激光共聚焦显微镜测定VEC内Fluo-3的荧光强度代表钙离子浓度。结果VEC分别经过缺氧及AngⅡ损伤后,细胞内钙离子浓度明显升高(P<0.01);缺氧条件下AngⅡ可引起VEC钙离子浓度进一步升高(P<0.01);金钠多可抑制细胞内钙离子浓度的升高,但各金钠多保护组的钙离子浓度仍明显高于空白对照组(P<0.05或P<0.01)。结论缺氧及AngⅡ等损伤因素都可引起VEC内钙离子浓度明显升高;金钠多明显减轻上述损伤,减轻细胞内钙离子超载,从而发挥对细胞的保护作用。
Objective To study the effect of hypoxia and angiotesin Ⅱ （Ang Ⅱ ） on intracellular free calcium in vascular endothelial cells（VEC） and investigate the protection of ginaton（ginkgo biloba extract） on it. Methods VEC hypoxia-injured model was established,and then cultured VECs were divided into seven groups of control group, simple hypoxia group, hypoxia＋ginaton group, simple Ang Ⅱ group, Ang Ⅱ ＋ ginaton group, hypoxia＋ Ang Ⅱgroup, hypoxia＋Ang Ⅱ ＋ ginaton group, which were loaded with Fluo-3/AM. Intracellular Ca^2＋ concentration （[Ca^2＋ ] i） was detected by laser confocal microscopy. Results Compared with control group, [Ca^2＋ ]i significantly increased either in hypoxia group or in Ang Ⅱ group （P〈0.01）. This change was clearer in hypoxia＋ Ang Ⅱ group than that in the other groups （P〈0. 01）. [Ca^2＋ ／]]i change could he significantly lessened by ginaton, but [Ca^2＋]i of each ginaton-treated group was still higher than that of control group （P〈 0.05）. Conclusion Ang Ⅱcould significantly increase [Ca^2＋ ] i of VEC injured by hypoxia. Ginaton has a significant protective effect on VEC injured by hypoxia and Ang Ⅱ through decreasing the intracellular Ca^2＋ overload.
出处
《江苏医药》
CAS
CSCD
北大核心
2009年第1期84-86,共3页
Jiangsu Medical Journal
基金
海军后勤科研基金(00-3321)
