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谷胱甘肽巯基转移酶α1/α4(GSTA1/A4)是体内重要的解毒酶,可降低多种内、外源性毒性化合物的毒性.然而,胆汁淤积病人肝细胞内G STA1/A4的表达是下调的,下调机制尚不清楚.本研究通过肿瘤坏死因子α(TNFα)处理人肝癌细胞Hep G2细胞,利用实时荧光定量聚合酶链式反应(q PCR)和蛋白质印迹(Western blot)检测GSTA1/A4、核因子κB(NF-κB)和核因子E2相关因子2(Nrf2)的表达.发现TNFα在m RNA水平和蛋白质水平均抑制GSTA1/A4表达,且呈剂量与时间依赖关系.干扰NF-κB信号通路,可减弱T NFα对G STA1/A4表达的抑制作用.以上结果表明,在Hep G2细胞中,TNFα可通过激活N F-κB信号通路抑制G STA1/A4表达.
Glutathione S-transferase α1 / α4 (GSTA1 / A4), an important detoxification enzyme in the body, can reduce the toxicity of many endogenous and exogenous toxic compounds.However, the expression of G -STA1 / A4 in hepatocytes of patients with cholestasis Is down-regulated, the mechanism of down-regulation is not clear.In this study, human hepatocellular carcinoma Hep G2 cells were treated with tumor necrosis factor alpha (TNFα), and real-time quantitative polymerase chain reaction (qPCR) and Western blot were used to detect GSTA1 / A4, nuclear factor kappa B (NF-κB) and nuclear factor E2 (Nrf2), we found that TNFα inhibited GSTA1 / A4 expression at both mRNA and protein levels in a time-and dose- -κB signaling pathway, which can attenuate the inhibitory effect of T NFα on the expression of GSTA1 / A4.The above results show that TNFα can inhibit the expression of GSTA1 / A4 by activating NF-κB signaling pathway in Hep G2 cells.