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目的研究乙型肝炎病毒X蛋白(HBx)对过氧化物酶体增殖物激活受体(PPAR)-α的抑制作用,并探讨其中的内在机制。方法培养人肝癌细胞系HepG2,转染HBx表达质粒,Western blot方法检测PPAR-α、丝裂原活化蛋白激酶(MAPK,ERK1／2)和IкB蛋白的变化,凝胶迁移率实验检测核转录因子(NF)-кB蛋白的活性改变,分别加入MAPK和NF-кB特异性的抑制剂PD98059与吡咯烷二硫代氨基甲酸盐(PDTC),观察PPAR-α蛋白的变化。结果(1)HBx质粒转染HepG2后,与对照组相比,ERK2表达增加,NF-кB被激活,PPAR-α的表达下调；(2)阻断NF-кB后,NF-кB的活性下降,PPAR-α的表达增加；(3)阻断MAPK后,转染HBx表达质粒,NF-кB的活性下降,PPAR-α的表达增加。结论HBx抑制细胞核转录因子PPAR-α的表达,可能与ERK1／2-NF-кB激活有关。
Objective To study the inhibitory effect of hepatitis B virus X protein (HBx) on peroxisome proliferator-activated receptor (PPAR) -α and its underlying mechanisms. Methods Human hepatocellular carcinoma cell line HepG2 was cultured and transfected with HBx expression plasmid. The changes of PPAR-α, mitogen-activated protein kinase (MAPK, ERK1 / 2) and IκB protein were detected by Western blot. (NF) -kappaB protein, and then add MAPK and NF-кB inhibitor PD98059 and PDTC respectively to observe the changes of PPAR-α protein. Results (1) Compared with the control group, the expression of ERK2 was increased and the expression of PPAR-α was down-regulated after HBx plasmid was transfected into HepG2. (2) The activity of NF-κB decreased after blocking NF-κB (3) After blocking MAPK, the activity of NF-кB was decreased and the expression of PPAR-α was increased after transfection of HBx expression plasmid. Conclusion HBx can inhibit the expression of nuclear transcription factor PPAR-α, which may be related to the activation of ERK1 / 2-NF-кB.