安徽医科大学学报2012，Vol.47Issue(3)：257-261,5.
Kupffer细胞在果糖引起的非酒精性脂肪肝中的作用
Role of KupffeR cells in fructose-evoked non-alcoholic fatty liveR disease
摘要
Abstract
To investigate the role of Kupffer cells in fructose-evoked non-alcoholic fatty liver disease ( NAFLD ) . Methods Forty - eight mice were randomly divided into four groups : control group, fruct- ose group, Gadolinium chloride( GdCl3 ) group and GdCl3 + fructose group. In control group, mice had free drinking tap water. In fructose group,mice had free drinking tap water containing 30% fructose. In GdCl3 group,mice were free drinking tap water and administered with GdCl3( 10 mg/kg,ip ) twice a week. In GdCl3 + fructose group,mice were free drinking tap water containing 30% fructose and administered with GdCl3( 10 mg/kg,ip )twice a week. All mice were sacrificed after fed for ten weeks. Blood serum was collected for serum triglyceride( TG )measurement. Liver was collected for RT-PCR, Western blot and hepatic TG measurement, or fixed in neutral-buffered formalin for histological examination, or frozen-fixed in OCT mounting media for Oil red 0 staining. Results The level of serum and hepatic TG was significantly increased in mice fed with fructose solution as compared with those drinking plain tap water. An obvious hepatic lipid accumulation was determined by HE and Oil Red 0 staining in fructose-fed mice. The level of hepatic TG was significantly attenuated in mice fed with GdCl3 + fructose solution as compared with those drinking fructose solution. In addition, GdCl3 pretreatment prevented hepatic lipid accumulation. Chronic fructose drinking induced hepatic sterol regulated element-binding protein-1 c ( SREBP-1 c )activation. Chronic fructose drinking upregulated the expression of enzymes for TG synthesis, such as fatty acid synthase( FAS ), acetyl-CoA carboxylase( ACC )and stearoyl-CoA desaturase 1 ( SCD-1 ). GdCl3 pretreatment significantly attenuated SREBP-1 c activation and the expression of SREBP-1 c target genes. Conclusion The increased hepatic TG synthesis in fructose - fed mice is mainly attributed to hepatic SREBP-1 c activation. Kupffer cells activation play an important role on fructose-evoked SREBP-1 c activation and lipid accumulation.关键词
果糖/非酒精性脂肪性肝病/固醇调节元件结合蛋白-1c/Kupffer细胞Key words
fructose/ NAFLD/ SREBP-1 c/ Kupffer cells分类
医药卫生引用本文复制引用
朱仁敏,张程,陈熙,张莹,徐德祥..Kupffer细胞在果糖引起的非酒精性脂肪肝中的作用[J].安徽医科大学学报,2012,47(3):257-261,5.基金项目
国家自然科学基金(编号:81172711,30973544,81001480) （编号:81172711,30973544,81001480）
安徽省自然科学基金(编号:090413142) （编号:090413142）
安徽省高校省级自然科学研究重点项目(编号:KJ2011A159) （编号:KJ2011A159）
安徽医科大学校科学研究基金(编号:2010xkj016) （编号:2010xkj016）
