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机构地区:[1]广东省深圳市第二人民医院心血管内科,510089 [2]深圳市盐田区人民医院
出 处:《岭南急诊医学杂志》2015年第1期3-4,10,共3页Lingnan Journal of Emergency Medicine
摘 要:目的:探讨血管紧张素-(1-7)[Ang-(1-7)]对心肌细胞缺血再灌注损伤(I/R)的影响及其可能机制。方法:提取乳鼠原代细胞,按缺氧4 h后再灌注2 h的条件建立I/R模型。提前20 min加入10-8、10-7、10-6、10-5mmol/l的Ang-(1-7)作为预处理,并随机分为对照组、I/R组、Ang-(1-7)组、替米沙坦组、血管紧张素Ⅱ组、Ang-(1-7)+替米沙坦组及Ang-(1-7)+血管紧张素Ⅱ组,使用CCK-8法检测心肌细胞存活率。结果:10-5mmol/L浓度的Ang-(1-7)的预处理能让细胞存活率提高到77.65%。与I/R组相比,Ang-(1-7)组、Ang-(1-7)+替米沙坦组及Ang-(1-7)+血管紧张素Ⅱ组心肌细胞存活率均显著提高,但各组间均无明显差异。结论 :Ang-(1-7)减少心肌细胞在I/R中的损伤,但该保护机制与血管紧张素受体Ⅱ无关。Objective :To explore the effects of Ang-(1-7) on ischemia-reperfusion injury in an isolated rat myocytes and its possible mechanisms. Methods : Myocytes from neonatal rat were isolated and reperfusion 2 h after anoxic 4 h to establish model of ischemia-reperfusion(I / R).Myocytes were pretreated by Ang-(1-7)as the concentration of 10-8mmol / l、10-7mmol / l、10-6mmol / l、10-5mmol / l before 20 min and randomly divided into following groups :control group,I / R group, Ang-(1-7) group, telmisarton group, angiotensin Ⅱ group, Ang-(1-7)+telmisarton group,and Ang-(1-7) +angiotensin Ⅱ group. Viabilities of myocytes were measured by CCK-8. Results :In established ischemia-reperfusion model,the myocytes viability in group with 10-5 mmol / L Ang-(1-7) was significantly increased to 77.65%. Compared with I / R group, the myocytes viability significantly increased,but the difference between Ang-(1-7) group,Ang-(1-7) + telmisarton group,and Ang-(1-7) + angiotensin Ⅱ group had no statistical significance.Conclusions : Ang-(1-7) reduced the I / R injury and improved myocytes viability and this effect is not mediated by angiotensin receptor Ⅱ.
关 键 词:血管紧张素-(1-7) 肾素-血管紧张素系统 缺血再灌注
分 类 号:R542.2[医药卫生—心血管疾病]
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