脂质堆积及再生能力低下制约着脂肪肝作为活体肝移植供体的应用。LXRα是参与脂质代谢和细胞增殖的重要调控因子。小鼠肝脏部分切除术后，LXRα信号通路的关闭对维持细胞内充足的胆固醇水平，保证肝脏再生至关重要。我们以往的研究发现羟基类固醇硫酸基转移酶（SULT2B1b）及其介导的硫酸化反应产物可以通过抑制LXRα信号通路降低体内外脂质水平并促进正常肝细胞的增殖。因此，我们提出SULT2B1b可以通过调节LXRα信号通路，降低脂肪肝内脂质水平并促进脂肪肝细胞再生。基于此，本课题拟在非酒精性脂肪肝小鼠模型中，研究SULT2B1b过表达对脂肪肝大部切除后肝再生的影响；利用LXRα-/-敲基因小鼠，探讨LXRα信号通路在上述过程中的作用；在体外脂肪肝细胞模型中，应用siRNA干扰技术反证SULT2B1b对脂肪肝细胞再生的影响。本课题的研究结果将阐明SULT2B1b在脂肪肝大部切除后再生中的作用及机制。

Lipid accumulation and impaired regeneration capacity limit the application of fatty liver as donors for living donor liver transplantation. LXRα is an important regulatory factor involved in lipid metabolism and cell proliferation. Turning off LXR-transcriptional pathways is crucial to guaranteeing the requisite intracellular cholesterol levels of regenerating hepatocytes. We have shown that oxysterol sulfotransferase (SULT2B1b) and the product of SULT2B1b decrease lipids and increases hepatic cell proliferation in vitro and in vivo via inhibiting LXRα signaling pathway. Therefore, we hypothesize that SULT2B1b decreases hepatic lipids and promotes fatty liver regeneration after partial hepatectomy (PH) via LXRα signaling. In the present study, firstly, we will investigate the effect of SULT2B1b on fatty liver regeneration after PH in mouse model of nonalcoholic fatty liver disease (NAFLD); secondly, we will explore the role of LXRα in the process above by using LXRα-/- and mouse model; finally, we will confirm the effect of SULT2B1b on fatty liver regeneration by using RNA interference in vitro fatty liver cell model. These results will demonstrate the effect and mechanism of SULT2B1b on fatty liver regeneration.