HBx与肝细胞脂肪变性关系及可能机制的细胞学研究

Relationship and Possible Mechanism of Hepatitis B Virus X Protein Expression with Hepatic Steatosis

从细胞水平探讨乙型肝炎病毒X蛋白(hepatitis B virus X protein,HBx)与肝细胞脂肪变性的关系,并探讨其可能分子机制。油红O染色及细胞内甘油三酯含量测定鉴定HepG2.2.15细胞和HepG2细胞的脂变程度;Western blotting检测HBx,肝X受体(liver X receptor alpha,LXRα)及脂肪酸合成酶(fatty acid synthase,FAS)蛋白的表达。结果显示,C2.2.15组细胞脂变程度较CG2组细胞重。O2.2.15组细胞在24,48及72h的脂变程度及TG含量均较同一时间段的OG2组增加;Western blotting结果显示,HepG2.2.15细胞内有HBx蛋白表达,而HepG2细胞则无此蛋白表达;C2.2.15组细胞LXRα及FAS蛋白表达强度较CG2组细胞高。HBx蛋白与肝细胞脂肪变性存在密切的关系,其机制可能与HBx/LXRα/FAS信号通路有关。

Hepatic steatosis occurs in roughly a quarter to a half of patients with chronic hepatitis B （CHB） or chronic hepatitis C （CHC）. However, the specific functions of hepatitis B virus X protein （HBx） , which include potential mechanisms of the regulation of hepatic adipogenic and lipogenic genes, remain to be poorly understood. Here we explored the HBx might be involed in HBV-associated hepatic steatosis via interacting with LXRα and FAS. Lipid accumulation in HepG2.2. 15 and HepG2 cells was observed by oil red O staining and TG content detection. HBx, LXRc（ and FAS protein expression levels were measured by western blotting. Results showed that compared with the HepG2 cells, lipid droplets and the TG content were markedly increased in HepG2.2.15cells. The HBx was only existed in HepG2.2. 15 cells. The expression of LXRα and FAS proteins in HepG2. 2. 15 cells was obviously higher than that of HepG2 cells. Our results demonstrated that HBx interacts with LXRα, thereby resulting in the up-regulation of FAS which could be a putative molecular mechanism of HBV-associated hepatic lipid accumulation.