ABCG1在肿瘤坏死因子α诱导的氧化应激中的机制研究

发布时间：2018-06-26 02:47

本文选题：三磷酸腺苷结合盒转运体G + 氧化应激　；参考：《中国现代医学杂志》2017年11期

【摘要】：目的探讨三磷酸腺苷结合盒转运体G1(ABCG1)在肿瘤坏死因子α(TNF-α)诱导的氧化应激中的作用及可能的机制。方法人脐静脉内皮细胞被特异性ABCG1 si RNA或ABCG1过表达质粒转染或使用LXR(肝X受体)激活剂T0901317预处理,随后给予肿瘤坏死因子(TNF-α)干预12 h。采用DCFHDAAM(2’7’-二氯荧光双乙酸盐)荧光探针检测细胞内活性氧簇(ROS)的水平,分光光度仪测量还原型烟酰胺腺嘌呤二核苷酸磷(NADPH)氧化酶活性,实时荧光定量聚合酶链反应法(q RT-PCR)和Western blot检测内皮细胞NADPH氧化酶亚型非吞噬细胞氧化酶4(NOX4)表达及超氧化物歧化酶(SOD)的表达。结果 ABCG1表达上调抑制TNF-α诱导的氧化应激,同时抑制促氧化应激的NADPH氧化酶的活性和NOX4的表达,促进抗氧化的SOD表达。相反,ABCG1表达下调进一步诱导ROS的产生,诱导NADPH氧化酶的活性和NOX4的表达,抑制SOD1表达。结论 ABCG1通过调节NADPH氧化酶/SOD抑制TNF-α诱导的氧化应激。
[Abstract]:Objective to investigate the role of adenosine triphosphate binding cassette transporter G1 (ABCG1) in oxidative stress induced by tumor necrosis factor 伪 (TNF- 伪) and its possible mechanism. Methods Human umbilical vein endothelial cells were transfected with specific ABCG1si RNA or ABCG1 overexpression plasmid or pretreated with LXR (liver X receptor) activator T0901317, then treated with tumor necrosis factor (TNF- 伪) for 12 h. The level of reactive oxygen species (Ros) in cells was detected by DCFHDAAM (2HDAAM) fluorescence probe, and the activity of NADPH oxidase was measured by spectrophotometer. The expression of NADPH oxidase subtype non-phagocyte oxidase 4 (NOX4) and superoxide dismutase (SOD) in endothelial cells were detected by real-time fluorescence quantitative polymerase chain reaction (Q RT-PCR) and Western blot. Results ABCG1 up-regulated the oxidative stress induced by TNF- 伪, inhibited the activity of NADPH oxidase and NOX4, and promoted the expression of antioxidant SOD. On the contrary, the down-regulation of ABCG1 expression further induced the production of Ros, the activity of NADPH oxidase and the expression of NOX4, and inhibited the expression of SOD1. Conclusion ABCG1 inhibits oxidative stress induced by TNF- 伪 by regulating NADPH oxidase / SOD.
【作者单位】：西安交通大学医学院第二附属医院心内科;
【基金】：国家自然科学基金(No:81100210)
【分类号】：R54

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