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ABCG1在腫瘤壞死因子α誘導的氧化應激中的機制研究

發(fā)布時間:2018-06-26 02:47

  本文選題:三磷酸腺苷結合盒轉運體G + 氧化應激。 參考:《中國現代醫(yī)學雜志》2017年11期


【摘要】:目的探討三磷酸腺苷結合盒轉運體G1(ABCG1)在腫瘤壞死因子α(TNF-α)誘導的氧化應激中的作用及可能的機制。方法人臍靜脈內皮細胞被特異性ABCG1 si RNA或ABCG1過表達質粒轉染或使用LXR(肝X受體)激活劑T0901317預處理,隨后給予腫瘤壞死因子(TNF-α)干預12 h。采用DCFHDAAM(2’7’-二氯熒光雙乙酸鹽)熒光探針檢測細胞內活性氧簇(ROS)的水平,分光光度儀測量還原型煙酰胺腺嘌呤二核苷酸磷(NADPH)氧化酶活性,實時熒光定量聚合酶鏈反應法(q RT-PCR)和Western blot檢測內皮細胞NADPH氧化酶亞型非吞噬細胞氧化酶4(NOX4)表達及超氧化物歧化酶(SOD)的表達。結果 ABCG1表達上調抑制TNF-α誘導的氧化應激,同時抑制促氧化應激的NADPH氧化酶的活性和NOX4的表達,促進抗氧化的SOD表達。相反,ABCG1表達下調進一步誘導ROS的產生,誘導NADPH氧化酶的活性和NOX4的表達,抑制SOD1表達。結論 ABCG1通過調節(jié)NADPH氧化酶/SOD抑制TNF-α誘導的氧化應激。
[Abstract]:Objective to investigate the role of adenosine triphosphate binding cassette transporter G1 (ABCG1) in oxidative stress induced by tumor necrosis factor 偽 (TNF- 偽) 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- 偽) 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- 偽, 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- 偽 by regulating NADPH oxidase / SOD.
【作者單位】: 西安交通大學醫(yī)學院第二附屬醫(yī)院心內科;
【基金】:國家自然科學基金(No:81100210)
【分類號】:R54

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