谷胱甘肽巰基轉移酶α1/α4(GSTA1/A4)是體內重要的解毒酶,可降低多種內、外源性毒性化合物的毒性.然而,膽汁淤積病人肝細胞內G STA1/A4的表達是下調的,下調機制尚不清楚.本研究通過腫瘤壞死因子α(TNFα)處理人肝癌細胞Hep G2細胞,利用實時熒光定量聚合酶鏈式反應(q PCR)和蛋白質印跡(Western blot)檢測GSTA1/A4、核因子κB(NF-κB)和核因子E2相關因子2(Nrf2)的表達.發(fā)現(xiàn)TNFα在m RNA水平和蛋白質水平均抑制GSTA1/A4表達,且呈劑量與時間依賴關系.干擾NF-κB信號通路,可減弱T NFα對G STA1/A4表達的抑制作用.以上結果表明,在Hep G2細胞中,TNFα可通過激活N F-κB信號通路抑制G STA1/A4表達.

【文章頁數(shù)】：9 頁

【文章目錄】：
1 Materials and methods
    1.1 Animal studies
    1.2 Hep G2 cells culture and treatment
    1.3 Cell viability analysis
    1.4RNA extraction and quantitative real-time polymerase chain reaction(q PCR)
    1.5Protein extraction and Western blotting analysis
    1.6 Statistical analysis
2 Results
    2.1 Reduction of Gst levels in the liver of BDL rats
    2.2 The bile acid content did not correlate with GSTA1 and GSTA4 expression in Hep G2 cells
    2.3 GSTA1 and GSTA4 expression in Hep G2cells was repressed by TNFα
    2.4 TNFαactivated NF-κB signaling and did not repress Nrf2 protein expression
    2.5 Inhibition of NF-κB activation attenuated TNFα-mediated decrease in GSTA1 and GSTA4expression
3 Discussion



本文編號：3998391