Objective To investigate the effect of tamoxifen(TAM) on steatosis in HepG2 cells in vitro and on the expression of key regulators involved in lipid metabolism in the cells. Methods A cell model of steatosis was induced in HepG2 cells in vitro with oleic acid (OA) at 50 μmol/L;HepG2 cells were then subjected to dif-ferent concentrations of TAM (5 to 20 μmol/L) at the presence of OA for 72 h;Intracellular lipid accumulation was assessed by oil red O staining and measurement of triglyceride;The expression of sterol regulatory element-binding protein-1c(SREBP-1c),fatty acid synthase(FAS),steroyl-CoA desaturase(SCD),carnitine palmitoyltrans-ferase 1(CPT1)and mitochondrial trifunctional protein(MTP)was determined by Western blot;Cell viability was de-tected by cell counting Kit-8 assay. Results After incubation for 72 h,the intracellular triglyceride in control group was (16.53±0.17) mg/100 mg protein,similar to that of cells treated with 5μmol/L TAM,however,the intra-cellular triglyceride was increased by 31%[(21.57±0.16) mg/100 mg protein] and 44%[(23.82±0.44) mg/100 mg protein] in cells treated with 10 μmol/L and 20 μmol/L of TAM,respectively(P<0.05);TAM treatment(5 to 10 μmol/L) significantly increased the expression of SREBP-1c,FAS,SCD and MTP without affecting the expression of carni-tine palmitoyltransferase 1 (CPT1) in HepG2 cells;TAM did not affect HepG2 viability. Conclusions TAM pro-motes OA-induced cell steatosis,probably by up-regulation of SREBP-1c,FAS and SCD,thus increases fatty acid synthesis in the cells.

Objective: To observe the effect of rhein and emodin on the proliferation of human renal tubular epithelial cell line( HK-2) and the activities of TGF-β1gene promoter. Methods: Effects of rhein and emodin on proliferation of HK-2 were analyzed by MTT; different lengths of human TGF-β1gene and CAT as reporter gene were constructed and were transferred into HK-2 RMC by transfection reagent. The effects of rhein and emodin( 1 μg / ml,10 μg / ml,50 μg / ml and 100 μg / ml) on the plasmid were determined by CAT-ELISA. Results: Rhein and emodin of different concentrations had regulatory effect on the proliferation of HK-2( P < 0. 01),and with dose compliance; rhein and emodin at 1 μg / ml and 10 μg / ml didn't inhibit the activities of phTGF 2. 14. Rhein and emodin at 50 μg / ml markedly inhibited the activities of ph TGF 2. 14,and the inhibition ratio was 38. 0% and 36. 0%,was different from the control group( P < 0. 01). Conclusion: Rhein and emodin have regulatory effect on the proliferation of HK-2. Rhein and emodin at 50 μg / ml have regulatory effect on the activity of TGF-β1gene promoter.

Objective To investigate the influence of whey proteins(WP) on serum lipid metabolism and hepatic fatty infiltration changes in rats with nonalcoholic fatty liver disease(NAFLD).Methods 35 SD rats were randomly divided into control(n=12),model(n=11) and the therapeutic groups(n=12).The control group were fed with normal diet,and the other two groups were fed with high-fat diet.Meanwhile,the therapeutic group were treated with WP(100mg/ml,0.5ml/d).All rats were sacrificed at the end of six weeks.The pathological changes in livers in all rats were pathologically evaluated with HE stain,and the serum biochemistry index was also measured.Results Compared with the control group,the degree of fatty and inflammation were more serious in the model group,while oral administration of WP reduced the final body and liver weights of rats;the alanine transaminase was 34.8±5.6U/l,and serum triglyceride level was 0.2±0.1mmol/l in WP group,obviously reduced as compared to those in model group;liver histology showed an improvement of fatty infiltration in therapeutic group;the NAFLD activity score was significantly improved from 6.2±0.9 to 2.9±1.4(P<0.01) in WP group.Conclusions The obtained results indicate that WP play a possible role in the regulation of liver biochemistries in the rat with NAFLD.The regulatory effect of WP is accompanied by an improvement in fatty infiltration and hepatic inflammation.