目的探讨血管紧张素-(1-7)[Ang-(1-7)]对血管紧张素Ⅱ(AngⅡ)致内皮细胞损伤的保护作用。方法体外培养的ECV-304内皮细胞株,随机分为4组:(1)对照组:单纯DMEM培养基培养;(2)AngⅡ组:单纯DMEM培养基,加入AngⅡ,终浓度为10-7mol/L;(3)Ang-(1-7)组:单纯DMEM培养基,加入Ang-(1-7),终浓度为10-7mol/L;(4)混合组:单纯DMEM培养基,加入Ang-(1-7)预处理30 m in,再加入AngⅡ,两者终浓度均为10-7mol/L。各组作用6,12,24 h,倒置相差显微镜下观察各时间点细胞的形态变化,收集细胞,流式细胞仪测定细胞内的活性氧,硝酸还原酶法测定上清液中的一氧化氮。结果AngⅡ组内皮细胞发生损伤性的形态学变化,活性氧生成增加,NO生成下降,与其他3组比较差异有显著性;Ang-(1-7)组与对照组比较,细胞形态没有变化,活性氧和NO含量差异无显著性;混合组与AngⅡ组相比,细胞损伤明显减弱,活性氧和NO含量与AngⅡ组比较差异有显著性,与对照组比较差异无显著性。结论Ang-(1-7)对AngⅡ导致的内皮损伤有保护性作用。
Therapeutic efficiency of advanced stage liver cancer is insufficiency,which has become the hot spot of *** observation found that prognosis of liver cancer with integrity amicula was *** is generally accepted that si...
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Therapeutic efficiency of advanced stage liver cancer is insufficiency,which has become the hot spot of *** observation found that prognosis of liver cancer with integrity amicula was *** is generally accepted that silicon dioxiode(SiO2) can induce pulmonary fibrosis,resulting in the formation of *** of SiO2 as embolism material induces hepatic fibrosis and forms the fibrosis amicula around the liver carcinoma,and then restrains the recurrence and metabasis of liver cancer,which has been turned into one of the aspect of liver carcinoma *** possible mechanisms of inducing hepatic fibrosis by SiO2 are peroxidative damage by free radical,releasing of active cytokines,or inducing cell apoptosis and the activation of HSC etc.
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