ObjectiveTo investigate the effect of amitriptyline on lipid deposition and biochemical metabolism in a cell model of nonalcoholic fatty liver disease (NAFLD) by regulating the acid sphingomyelinase (ASM)/ceramide (CE) pathway. MethodsHepG2 and L02 cells were cultured in vitro to establish a cell model of NAFLD. MTT colorimetry was used to measure cell proliferation rate, and oil red O staining was used to observe the change of lipid droplets in cells. In the experiment, the cells were divided into normal control group, model group, Ami group, TNFα group, and Ami+TNFα group. An automatic biochemical analyzer was used to measure the levels of triglyceride (TG) and total cholesterol (TC) in cells and the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in supernatant; ELISA was used to measure the levels of CE and ASM in cells; Western blot was used to measure the protein expression ASM in cells, and RT-PCR was used to measure the mRNA expression of ASM in cells. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the Turkey test was used for further comparison between two groups. ResultsCompared with the normal control group, the NAFLD model group had significant increases in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05). Compared with the model group, the Ami group had significant reductions in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05), and the TNFα group had significant increases in the protein and mRNA expression of ASM and the levels of CE, TG, ALT, and AST (all P＜0.05). Compared with the TNFα group, the Ami+TNFα group had significant reductions in the protein and mRNA expression of ASM and the levels of CE, TG, TC, ALT, and AST (all P＜0.05). ConclusionThe ASM/CE pathway promotes lipid accumulation and may lead to hepatocyte steatosis, and amitriptyline can alleviate lipid deposition in NAFLD hepatocytes by inhibiting the ASM/CE pathway.

【Objective】 To investigate the inhibitory effect of BFD-6b on colorectal cancer cell growth and its preliminary mechanism. 【Methods】 The inhibitory effect of BFD-6b on the growth of various tumor cells （SW480， MCF-7， T47D， SMMC-7721， BEL-7402， 97H， SK-HEP-1， H460， H1299， A549， MS751， and HELA） was investigated by MTT assay； the effect of BFD-6b on apoptosis and cell cycle was detected by flow cytometry； the effect of BFD-6b on the expressions of cell cycle-related proteins and apoptosis-related proteins was examined by Western blotting. 【Results】 BFD-6b inhibited the proliferation of different cancer cells such as SW480， MCF-7， H460， H1299， A549， and HELA. Among all of them， SW480 cells were most sensitive to BFD-6b， and the IC50 value was 7.09 μmol/L. Furthermore， BFD-6b could inhibit the growth of another three colorectal cell （SW620， Lovo， and HCT116 cells）； the IC50 values were 7.23， 8.08 and 8.96 μmol/L， respectively. BFD-6b could downregulate the amount of cyclinD1， cyclinE， and cell cycle-dependent kinase CDC2， thereby arresting the cell cycle at G1 phase. Also， BFD-6b downregulated the expressions of anti-apoptotic proteins Mcl-1 and Bcl-2， and upregulated the expressions of pro-apoptotic proteins BAK and BAX， thus inducing apoptosis of SW480 cells. 【Conclusion】 BFD-6b arrests SW480 cells at G1 phase by downregulating the expressions of cyclinD1， cyclinE and CDC2， and induces SW480 cell apoptosis by downregulating the expressions of Mcl-1 and Bcl-2 and upregulating the expressions of BAK and BAX， thereby inhibiting the proliferation of colorectal cancer SW480 cells.