6 ml/kg), group B (po alpha-naphthylisothiocyanate(ANIT) 50 mg/kg+ ip saline 0.6 ml/kg), group C (po ANIT as group B + ip SAMe 60 mg/kg), group D (po ANIT as group B+ ip SAMe vehicle as group A). Animals of each group were treated at hour 24, 48, 72, and 96 post ANIT gavage, 3 rats each time, respectively.TBA,CHOL, ALT, AST, GGT, ALP, TB, DB at each time point each group were determined.

Results: Significant decrease of TBA,CHOL,ALT,AST, GGT,ALP,TB, DB were observed in group C compared with group B and D, but no significant difference between group A and B. The level of TBA,CHOL, ALT, AST, GGT, ALP, TB, DB is highest at the time of 72 h, and lowest at the time of 24 h ,which is affected by ANIT. Conclusion: SAMe Metabolism inhibitor can well recover the damage of IHC rats , and the effect is better as the time going. Key Word(s): 1. SAMe; 2. IHC; Presenting

Author: SONG ZHANG Additional Authors: JING HUO, LIPING TONG, LI DING, WENQIANG FENG, JINGBO MA, MEILING DING, XIAOKE HAO, JIANHONG WANG, YONGZHAN NIE Corresponding Author: SONG ZHANG, YONGZHAN NIE Affiliations: Xijing Hospital of Digestive Disease; Xijing Hospital of Clinic Diagnostic Laboratory Objective: Non-alcoholic Fatty Liver Disease (NAFLD) can develop into serious liver disease and metabolic syndrome BMS-907351 nmr with a high incidence of 20%. Recent studies have shown that SirT1, a highly conserved NAD+-dependent protein deacetylase, can regulate liver lipid metabolism associated proteins, but the detailed mechanism is unknown. Based on approaches of proteomics and functional genomics, using spontaneous occurrence of fatty liver SirT1-LKO animal model, this study is aimed at screening non-alcoholic fatty liver disease associated proteins, and clarifying how SirT1 regulates these proteins involved in NAFLD. Methods: SIRT1 LKO mice and control mice were fed ad libitum either control or a high-fat diet providing 60% Kcal for eight weeks. Blood samples of the four groups mice were collected for testing plasma levels

of total cholesterol (TC) and triglyceride (TG). 上海皓元 The livers were removed and fixed in 10% neutral buffered formalin for HE staining. Extracting the RNA samples of the four groups mice liver tissue for microarray analysis. Preparation the liver protein samples of the four groups mice liver tissue for iTRAQ MS. Results: SIRT1 LKO mice accumulate more lipids in the liver under high-fat diet by HE staining. Using microarray analysis, we found 67 genes involved in lipid metabolism changed under different diet between SirT1-LKO and control mice. Using iTRAQ MS, we identified 17 proteins involved in lipid metabolism.we also analysed the lipid metabolic pathway afftecd by SirT1, and found that Wnt signaling pathway, Glycerolipid metabolism and Pathways in cancer were changed.