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首页> 外文期刊>Cellular Physiology and Biochemistry >Hepatitis B Virus Core Antigen Stimulates IL-6 Expression via p38, ERK and NF-?oB Pathways in Hepatocytes
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Hepatitis B Virus Core Antigen Stimulates IL-6 Expression via p38, ERK and NF-?oB Pathways in Hepatocytes

机译：乙型肝炎病毒核心抗原通过p38，ERK和NF-？oB途径刺激肝细胞中IL-6的表达

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>Background: Hepatitis B virus (HBV) causes both acute and chronic liver injury. Viral proteins are involved in the pathological progress. Hepatitis B core antigen (HBcAg), a component of viral nucleocapsid, is not only essential for HBV lifecycle, but also exhibits strong immunogenicity. The cytoplasmic location of HBcAg in liver biopsy is associated with liver injury and inflammation, but the exact mechanisms remain to be elaborated. Methods: Huh7, SMMC-7721 and L-02 cells were transfected with pEGFP-N1-HBcAg to establish an intracellular HBcAg expression model. The mRNA and protein levels of Interleukin (IL)-6 were detected by qPCR and ELISA respectively. The signaling pathway-related proteins were investigated by western blot and immunofluorescence assay. Results: HBcAg increased the expression and secretion of IL-6 through activating extracellular signal-related kinase (ERK), p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-?oB). These activations can be blocked by specific inhibitors of the three pathways. Conclusions: HBcAg actives p38, ERK1/2 and NF-?oB to enhance the production of IL-6 in hepatocytes. This provides a molecular mechanism to explain the association of cytoplasmic HBcAg with severe liver injury and inflammation.
机译：> 背景： 乙肝病毒（HBV）引起急性和慢性肝损伤。病毒蛋白参与病理过程。乙型肝炎核心抗原（HBcAg）是病毒核衣壳的组成部分，不仅是HBV生命周期必不可少的，而且具有很强的免疫原性。肝活检中HBcAg的胞质位置与肝损伤和炎症有关，但确切机制尚待阐明。 方法： 用pEGFP-N1-HBcAg转染Huh7，SMMC-7721和L-02细胞，建立细胞内HBcAg表达模型。分别通过qPCR和ELISA检测白细胞介素（IL）-6 的mRNA和蛋白质水平。通过蛋白质印迹和免疫荧光法研究了信号通路相关蛋白。 结果： HBcAg通过激活细胞外信号相关激酶（ERK），p38丝裂原活化蛋白激酶（p38 MAPK）和核因子来提高IL-6的表达和分泌。 -κB（NF-κB）。这些激活可以被这三种途径的特异性抑制剂所阻断。 结论： HBcAg激活p38，ERK1 / 2和NF-αoB以增强肝细胞中IL-6的产生。这提供了解释细胞质HBcAg与严重肝损伤和炎症的关联的分子机制。

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