Objective To investigate the effect of the lack of intestinal bile on liver regeneration after hepatectomy.Methods The model of interference with intestinal bile acid metabolism in rats was established by feeding rats with 0.2% cholic acid(cholic acid loading group), 2% cholestyramine resin(lack of bile group)and feeding the standard diet as the control group.Liver regeneration was compared among the 3 groups at 0, 1, 2, 3, and 7 d after 70% partial hepatectomy(PH)in rats and mRNA expression of the rate-limiting enzyme of bile acid biosynthesis(CYP7a1)and farnesoid X receptor (FXR)were detected.Results The rate of liver regeneration was significantly lower on days 3 and 7after PH in the lack of bile group than in the other groups(P＜0.05).On day 1, the labeling indices of PCNA and Ki-67 in the lack of bile group(22.21% ±2.31%、 17.25 % ± 6.50 %)were lower than those in the cholic acid loading group(44.4%±4.92%、 30.83% ± 3.91%)and control group (38.74% ±6.42% 、27.04% ±7.22%)and the peaking of labeling indices was delayed.After PH, the mRNA expression of FXR was significantly lower in the lack of bile group than in other groups.However, CYP7al mRNA had a trend towards increase after PH and was higher than that in other groups.Conclusion Lack of intestinal bile results in delayed liver regeneration of normal rat liver accompanied by decreased expression of FXR mRNA after hepatectomy.

The Farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily and has emerged as a key player in the control of multiple metabolic pathways. Bile acids are the major endogenous ligands for FXR, and by activating FXR have a variety of target genes, many of which are geared toward pre- venting synthesis and uptake and promoting excretion of bile acids. Here we summarized the latest results from studies on FXR target genes and functions in bile acids metabolism in this article.

Objective To study the effect of somatostatin on the Proliferation in Human HepG2 Cells and the Level of Gene p16. Methods The cell line HepG2 were divided into 3 groups: control groupA, low concentration group B and high concentration group C. The flow cytometry (FCM) was used to detect phase distribution of the cycles and detect the expression of p16 gene by using RT-PCR. Results Human HepG2 cells affected 24 hours later by different density SST, using FCM, we discovered that the G1 cell cycles of each A group, B group, C group occupied the proportion respectively is (51.41±3.27)%, (65.43±3.41)%, (69.02±3.75)%, that the S cell cycles is (36.86±2.31)%, (20.34±2.52)%, (18.50±3.09)%, that the G2 cell cycles is (11.46±1.96)%, (14.23±3.83)%, (12.48±3.18)%. Compare to the control groupA, the G1 cell cycles of groupB and group C were increased obviously. But the S cell cycles relatively reduced. The levels of p16 gene were expressed in each group detected by RT-PCR, but B group and C group expressed obviously. Conclusion The inhibited mechanism of somatostatin for HepG2 was expressed probably by improving levels of p16.

The liver regeneration is closely related to the bile acids. To avoid the toxic effects of bile acids on hepatocyte, the state of bile secretion, the rate-limiting enzyme of the bile acid synthesis, bile acids composition as well as the transporter changes at the process of liver regeneration. In vivo and in vitro experiments show that bile acids can promote liver cell proliferation, liver regeneration may be related to the signal which is released under the bile acid imbalance. The relationship between the liver regeneration and bile acid metabolism has an important practical significance in liver regeneration.

OBJECTIVE: To investigate the perception of surgeon to ADR reporting system. METHODS: Postal questionnaire was used for survey among 300 surgeons in November 2009. RESULTS & CONCLUSIONS: Surgeons mastered a little knowledge about ADR reporting system. More than 50% of surgeons took one-side view on national ADR monitoring with ADR reporting rate of 42.8%. 57.2% of surgeons hadn’t received relevant training. It is suggested that surgeons receive training and education about the knowledge of ADR reporting.

Objective To explore the effect of FTY720 on human hepatocellular carcinoma cell line HepG-2 of invasion ability. Methods HepG-2 cells were cultured,and divided into 4 groups,namely control and FTY720 (0.05 g/ml,0.10 g/ml,0.15 g/ml) groups.The cell invasion ability was observed by the cell invasion assay.mRNA expression of MMP-2,MMP-9 was measured by RT-PCR.MMP-2,MMP-9 protein expression was measured by ELISA method.Results The invasive ability of cancer cells in each group significantly weaken,with the FTY720 concentration increased.The number of control group was (110±3)(P<0.05),the number of O.05 g/ml FRY720 treatment group cells was (74±4),while the number of cells of O.10 g/ml,0.15 g/ml the drug treated group,Was (42±3),(25±5)(P<0.01).Compared with control group,the MMP-2,MMP-9 expression of different concentrations of FTY720 groups decreased significantly (P<0.05).As the expression of FTY720 concentration increased,the MMP-2,MMP-9 expression decreased (P<0.01).Compared with control group,the MMP-2,MMP-9 protein expression of different concentrations of FTY720 groups decreased significantly (P<0.05), but the protein expression and concentration of FTY720 is inversely proportional in a certain range. Conclusion The invasive ability of HepG-2 cells can be inhibited by FTY720,and with FTY720 concentration increased,the invasive ability decreased gradually.One of the mechanisms may be related to reduce the MMP-2,MMP-9 protein and gene expression.

Objective To investigate the effect of sodium demethylcantharidate injection on adherence,invasion and metastasis and to investigate the related mechanism in human hepatocarcinoma cell line HepG2.Methods Adherence ability,migration and invasion of HepG2 cells inhibited by sodium demethylcantharidate injection were assessed by MTT and Transwell techniques.Expression levels of MMP-9 protein in HepG2 cells were determined by immunohistochemistry.Results The number of adhesion,migration and invasion of HepG2 cells were significantly lower in sodium demethylcantharidate injection group than those in the control group (P ＜ 0.05).HepG2 cells co-incubated with sodium demethylcantharidate injection in the concentration of 0.25 μg/ml for 30,60,90 and 120 min showed higher cell adhesion than the control group.The adhesion inhibition ratios were 48.11％,33.81％,28.97 ％ and 16.83 ％,respectively.The migration and invasion inhibition rates were 64.19 ％ and 58.19 ％.With concentration of sodium demethylcantharidate injection to increasing,expression levels of MMP-9 protein in HepG2 cells more and more lower than control group.Conclusion The adherence,migration and invasion abilities of HepG2 cells are markedly inhibited by sodium demethylcantharidate injection,the mechanisms is possible related to the expression levels of MMP-9 protein.

Objective To investigate the effect of salvia miltiorrhiza (SM) on the expression of Bcl 2?Bax and hepatocyte apoptosis in hepatic preservation and reperfusion in a murine model.Methods The model of the preservation reperfusion of isolated rat liver was established. Bcl 2?Bax expression of the liver tissue and hepatocyte apoptosis were studied respectively by flow cytometry and in situ terminal deoxynucleotidyl transferase mediated dUTP FITC nick end labeling (TUNEL) technique. Results In SM treated group levels of Bcl 2 expression was significantly increased ( P

Objective To study the action of CNOT 7 (CCR4-NOT transcription complex subunit 7 human)gene and its mechanisms in the process of Vγ 9Vδ2T cell immunologic tolerance of HepG2 cells (Hepatoblastoma G2 Cell Line).Methods The shCNOT 7 (Recombinant plasmid of CNOT 7) and control vector shRNA were transfected into HepG2 cells.Vγ9Vδ2T cytokine stimulated each group before and after cell transfection,Cell apoptosis was detected by flow cytometry (FCM),CNOT 7 protein and STAT1,STAT3 expression level was detected by Western blot.CNOT 7,STAT1 and STAT3 protein expression levels of HepG2 liver cancer cell lines and L02 normal liver cell line was assayed by Western blot.Results When stimulated by Vγ9Vδ2T cytokine,the apoptosis rate of gene-knockdown group significantly improved from (7.55％ ±2.63％) to (20.59％ ±3.12％).Compared with L02 cells,the CNOT7 protein expression of HepG2 cells increased (F =28.76,P ＜ 0.01),STAT3 protein expression increased (F =110.29,P ＜ 0.01),while STAT1 protein expression was down-regulated (F =35.67,P ＜ 0.01).CNOT 7 knockout could induce HepG2 cells STAT1 expression (t =6.69,P ＜ 0.05).Conclusions CNOT 7 gene could induce HepG2 cells Vγ 9Vδ2T cellular immune tolerance.CNOT 7 knockout could reverse the Vγ 9Vδ2T cell immunologic tolerance of HCC.

The present study attempted to examine the effects of bile acid pool size on liver regeneration after hepatectomy. The rats were fed on 0.2% cholic acid (CA) or 2% cholestyramine for 7 days to induce a change in the bile acid size, and then a partial hepatectomy (PH) was performed. Rats fed on the normal diet served as the controls. Measurements were made on the rate of liver regeneration, the labeling indices of PCNA, the plasma total bile acids (TBA), and the mRNA expression of cholesterol 7alpha-hydroxylase (CYP7A1), farnesoid X receptor (FXR), and transcription factor c-Jun or c-fos. As compared with the normal and CA groups, the rate of liver regeneration was decreased on the day 3, and 7 after PH; the peak of the labeling indices of PCNA was delayed and the labeling indices were significantly reduced on the day 1; the TBA were also decreased on the day 1; the expression of FXR decreased but that of CYP7A1 increased at any given time; at the 1st, and 3rd h, the expression of c-Jun was declined in the cholestyramine group. The reduction in the bile acid pool size was found to delay the liver regeneration, which may be caused by the down-regulation of FXR and c-Jun expression.