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目的观察血管紧张素Ⅱ(AngiotensinⅡAⅡ)抑制人脐静脉内皮细胞株ECV304细胞的大电导钙激活钾通道(Maxi-conductancecalcium-activatedpotassiumchannelBKCa)效应与AⅡ受体、蛋白激酶C(ProteinKinaseCPKC)和一氧化氮(NitricOxideNO)的关系,以及中药银杏叶提取物Gingkoleafextract对AⅡ抑制BKCa效应的影响。方法细胞贴附式膜片箝技术。结果AⅡ受体拮抗剂saralasin(10-7mol/L)可对抗AⅡ(10-7mol/L)的抑制效应;PKC的激动剂佛波酯(5×10-8mol/LPhorbolester)可加重AⅡ的抑制效应;NO(10-10mol/L,sod-iumnitroprussideSNP)则削弱AⅡ的抑制作用。中药银杏叶提取物(800μg/ml)可激活BKCa并可对抗AⅡ的抑制效应。结论AⅡ对ECV304BKCa的抑制是由AⅡ受体介导的,PKC参与其中。NO与银杏叶提取物对ECV304BKCa免受AⅡ的抑制具有保护作用。
Objective To investigate the effects of Angiotensin Ⅱ A (AⅡ) on the proliferation of human umbilical vein endothelial cells (ECV304) and the expression of AⅡ receptor, protein kinase C (PKC) And Nitric Oxide (NO), as well as the effect of Ginkgo biloba extract (Ginkgo biloba extract) on AⅡ inhibit BKCa effect. Methods Cell attachment patch clamp technique. Results The inhibitory effect of AⅡ receptor antagonist saralasin (10-7mol / L) against AⅡ (10-7mol / L) was inhibited. PKC agonist phorbol ester (5 × 10-8mol / L Phorbolester) Inhibition effect; NO (10-10mol / L, sod-iumnitroprussideSNP) weakened A Ⅱ inhibitory effect. Ginkgo biloba extract (800μg / ml) can activate BKCa and antagonize the inhibitory effect of AⅡ. Conclusion The inhibition of AⅡ on ECV304BKCa is mediated by AⅡ receptor, and PKC is involved. NO and Ginkgo biloba extract on ECV304BKCa from A Ⅱ inhibition has a protective effect.