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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 observe the effect of angiotensin II (Ang II) on the calcium concentration in vascular endothelial cells (VEC) during hypoxia and to investigate the protective effect of Jin Nao Duo (Ginkgo biloba extract) on VEC. Methods VEC hypoxic injury models were established; the experiments were divided into blank control group, simple hypoxia group, hypoxia plus JinNaDuo protection group, simple AngII effect group, AngII plus JinNaDuo protection group, hypoxia plus AngII effect group, and deficiency. Oxygen plus AngII plus gold sodium protection group 7 groups. After each group of cells was loaded with Fluo-3/AM, the fluorescence intensity of Fluo-3 in VEC was measured by laser confocal microscopy to represent the concentration of calcium ions. RESULTS: After the VECs were injured by hypoxia and Ang II, the intracellular calcium concentration was significantly increased (P<0.01). Under hypoxic conditions, the calcium concentration of VECs was further increased by AngII (P<0.01). The intracellular calcium concentration increased, but the calcium concentration in the gold sodium multiprotection group was still significantly higher than that in the blank control group (P<0.05 or P<0.01). Conclusions Hypoxia and AngII and other damage factors can all cause the increase of calcium concentration in VECs. Jin Nadol can significantly reduce the above-mentioned damage, reduce the intracellular calcium overload, and exert its protective effect on cells.