HepG2细胞中TNFα通过NF-κB信号通路下调GSTA1/GSTA4表达

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HepG2细胞中TNFα通过NF-κB信号通路下调GSTA1/GSTA4表达
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作者单位:第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心,第三军医大学西南医院中国人民解放军胃肠病研究所胆汁淤积肝病中心
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基金项目:国家自然科学基金资助项目(81370560, 81570576, 81470850, 81470880)

Tumor Necrosis Factor Alpha Down-regulated Human GSTA1 and GSTA4 Expression Through The NF-κB Signaling Pathway in Human Hepatoma HepG2 Cells

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Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University,Cholestatic Liver Diseases Center, Institute of Gastroenterology of P.L.A., Southwest Hospital, Third Military Medical University

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This work was supported by grants from The National Natural Science Foundation of China (81370560, 81570576, 81470850, 81470880)

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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GSTA1/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HepG2细胞，利用实时荧光定量聚合酶链式反应(qPCR)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mRNA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TNFα对GSTA1/A4表达的抑制作用．以上结果表明，在HepG2细胞中，TNFα可通过激活NF-κB信号通路抑制GSTA1/A4表达.

Abstract:

Glutathione S-transferase Alpha1 and Alpha 4 (GSTA1 and GSTA4) are crucial for detoxifying a variety of endogenous and exogenous toxic compounds. However, GSTA1/4 expression is reduced in cholestatic patients. The molecular mechanism of GSTA1/4 down-regulation remains elusive. Here, we treated human hepatoma HepG2 cells with tumor necrosis factor alpha (TNFα) and measured the expression of GSTA1/4, nuclear factor kappa B (NF-κB) and NF-E2 related factor 2 (Nrf2) by quantitative real-time quantitative polymerase chain reaction (qPCR) and Western blotting. We found that expression of GSTA1/4 was repressed by TNFα at both the mRNA and the protein level in a dose- and time-dependent manner. Furthermore, inhibiting the NF-κB signaling pathway could attenuate the TNFα induced reduction in GSTA1/4 expression in the HepG2 cells. Our findings indicate that down-regulation of GSTA1/4 expression in HepG2 cells is likely triggered by TNFα and mediated by activation of the NF-κB signaling pathway.

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杨龙,熊志勇,张樑君,封欣禅,陈琨,李彦,程英,龙庆林,肖天利,陈磊,闫文慧,李灵欣,柴进,陈文生. HepG2细胞中TNFα通过NF-κB信号通路下调GSTA1/GSTA4表达[J].生物化学与生物物理进展,2016,43(8):801-809

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收稿日期:2016-03-10
最后修改日期:2016-05-25
接受日期:2016-06-16
在线发布日期: 2016-08-05
出版日期: 2016-08-20

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