乙型肝炎病毒X蛋白（HBx）可导致肝细胞脂肪化，确切机制尚未完全阐明。我们前期的研究表明，HBx 蛋白可促进肝型脂肪酸结合蛋白（L-FABP）及抑制NAD(P)H:醌氧化还原酶1（NQO1）基因转录和蛋白产生，而已有的研究表明L-FABP增高或NQO1下降可导致肝细胞脂肪化。本研究旨在探讨HBx 蛋白对这两种基因的调控机制及对肝细胞脂肪化的影响。对于L-FABP，首先确定HBx蛋白是否通过HNF3β和C/EBPα增强L-FABP基因转录，进而分析HBx蛋白对L-FABP介导的长链脂肪酸摄入及由此导致的肝细胞脂肪化的影响。对于NQO1，首先探讨HBx蛋白对NQO1基因启动子的甲基化修饰及机制；进而研究HBx蛋白对NQO1参与的反应性活性氧类（ROS）清除及线粒体稳定性的影响；最后评价HBx蛋白通过抑制NQO1基因转录对肝细胞脂肪化的影响。本研究有助于加深对HBx蛋白致肝细胞脂肪化机制的认识。

Hepatitis B virus X protein (HBx) causes hepatocyte steatosis, the mechanism involved is far from been fully elucidated. In our previuous study, we found that HBx could enhance the transcription of liver fatty acid binding protein (L-FABP), while reduce the transcription of (NAD(P)H dehydrogenase:quinone 1). Over expression of L-FABP or reduced expression of NQO1 was reported to be associated with hepatocyte steatosis. The aim of this study is to elucidate the effects of HBx on hepatocyte steatosis through gene regulation of L-FABP and NQO1. In the first part of the study, the HNF3β（Hepatocyte nuclear factor 3β）and C/EBPα（CCAAT/enhancer binding protein α）mediated regulation of L-FABP by HBx was investigated, and the effects of HBx on L-FABP-mediated long chain fatty acid trafficking and resulted hepatocyte steatosis were evaluated. In the second part of the study, effects of HBx on DNA methylation of NQO1 promoter region were firstly investigated, then the effects of HBx on NQO1-mediated clearing of the reactive oxygen species (ROS) and maitaining of the mitichondrial steady state, as well as the resulted hepatocyte steatosis were assessed. Our study will be helpful for deep understanding of the mechanism involved in HBx induced hepatocyte seatosis.