Many epidemiological data and study of experiment show that adminstration of NSAIDs in long term can prevent the carcinogenesis of colorectal cancer, its mecanism can be associated with the inhibition of PG which is produced by Cox 2 way, in addition, promoting apoptosis and anti oxidation were also one of the mecanisms of NSAIDs, the new selective Cox 2 inhibitor without gastrointestinal side effect would become the chemopreventive drugs of colorectal tumor.

Objective To investigate the expression of cellular FLICE/caspase-8 inhibitory protein(c-FLIP) in gastric cancer and its possible implications. Methods Forty-eight gastric cancer specimens and their normal counterparts were obtained. Western blot and immunohistochemistry were used to detect protein expression of c-FLIP. Semi-quantitative RT-PCR and TUNEL were used to measure c-FLIP mRNA levels and tissue apoptotic index, respectively. Results Mean levels of c-FLIP mRNA were significantly higher in gastric can-(cer) tissues than those in matched normal tissues (0.59?0.16 vs 0.24?0.13, P

Objective To investigate the correlation between phosphatidylinositol-3kinase(PI3′K)/serine/threonine kinase(Akt)/Forkhead like 1(FKHRL1)signaling pathway and chemoresistance in human gastric cancer cell line SGC7901.Methods From Jan.2004 to sep.2005,cells were exposed to doxorubicin with or without Wortmannin(a special inhibitor of PI3′K/Akt pathway)in Department of Gastroenterology the people's Hospital of when University.Cytotoxicity was assessed by determining cell survival with MTT.By Western blot analysis,the phosphorylation levels of FKHRL1 was evaluated in SGC-7901 cell.Results It was found that doxorubicin caused reduction of cell viability of SGC-7901 and induced phosphorylation of FKHRL1 in a time-dependent manner.Wortmannin enhanced the cell inhibitory efficiency of doxorubicin.Phosphorylation levels of FKHRL1 was significantly induced by Doxorubin in a time-dependent manner and was blocked by wortmannin.Conclusion Doxorubin may activate PI3′K/Akt signaling pathway and then induce phosphorylation of FKHRL1 in a time-dependent manner,which affects the chemoresistance of gastric cancer cell .However,Wortmannin enhances the chemotherapy sensitivity by suppressing this pathway.

0.05). The expression levels of Akt and pAkt proteins in cancerous tissues were 2.7-fold (P

Objective To investigate the effect of activation of protein kinase B(PKB) and Caspase-9 signal transduction pathway of human gastric cancer cells on the cell growth and chemosensitivity to etoposide.Methods The gastric cancer cells SGC7901 were treated with etoposide or etoposide plus PKB inhibitor Wortmannin at different time.The growth rates of gastric cancer cells SGC7901 and their sensitivity to etoposide were examined by 3-(4,5-dimethylthiazol-2,1)-2,5 diphanytetrazolium(bromide) assay.Apoptosis of gastric cancer cells was(detected) by flow cytometry.PKB activity was measured by(immunoprecipitation.) Caspase-3 expression and Caspase-9 activity were determined by Western bolt analysis.Results Etoposide induced apoptosis of SGC7901 cells and inhibited its survival effectively,which was much(weaker) 12 h after treatment.PKB(activity) became higher gradually,and Caspase-3 expression,Caspase-9(activity) significantly reduced at 12 h treated with etoposide.(Conversely),after pretreated with Wortmannin,PKB activity remarkably(reduced,) and Caspase-3(expression),Caspase-9 activity markedly increased.(Wortmannin) suppressed growth and potentiated (apoptosis) caused by etoposide.Potentiation of apoptosis by Wortmannin(correlated) with etoposide-induced PKB and Caspase-9 phosphorylation.Conclusions PKB and Caspase-9 signal transduction pathway promotes(human) gastric cancer cells survival and resistance to(chemotherapy.) PKB inhibitor can enhance sensitivity of gastric cancer cells to chemotherapy.

3. 0 cm in diameter). Methods During last 10 years, fifteen giant and symptomatic gastrointestinal lipomas were resected under endoscopy in our hospital. Of them, two giant lipomas with small stalk (

Objective To investigate the effects of EGB on hepatic fibrosis and expression of Activin A in rats with fibrosis.Methods From Oct.2004 to Apr.2005,the study was conducted in 30 adult male rats in the pepartment of Gastroenterology,the people's Hospital of Wuhan University.The rats were randomized into 3 groups:control group,model group and treatment group.Except the rats in the control group,others were induced to hepatic fibrosis by intraperitoneal injection of CCl_4 twice a week for 8 weeks.Those rats in the treatment group were intragastrically administered with EGB establish model of everyday.At the end of the 8th week,all rats were sacrificed.The samples of liver was staining with HE.The expression of Activin A was determined by immunohistochemistry and RT-PCR.Results The grade of fibrosis in EGB-treated groups were lower than that in the model group(P

Objective To study effects of hFRNK gene on phosphorylated p190RhoGAP expression and RhoA activation by mediated adenoviral vector in colorectal carcinoma cell Colo320WT stimulated with extrinsic gastrin17 in vitro.Methods AdEasyTMsystem was used to construct pAdhFRNK expressing human FRNK gene by recombination in E.coli.BJ5283.pCR3.1/GR plasmid expressing gastrin receptor CCK-2 was transfected into colonic carcinoma cell line Colo320 cells by LipofectamineTM2000 and expression stably CCK-2R clones was selected by G418(500 ?g/mL).The expression levels of gastrin receptor of Colo320 cells and the transfected cells Colo320WT were assayed by RT-PCR.Colo320WT cells were treated by 10～8 mol/L Gastrin17 for 0h and 12 h;and after Colo320WT cells were infected by pAdhFRNK(MOI:100)for 2 d,the cells were treated by Gastrin17 for 12 h again.The expression levels of phosphorylated p190RhoGAP of Colo320WT cells were assayed by immuniprecipation and western blot.RhoA activation was assayed by pull-down.using GST-Rhotekin-RBD followed by RhoA blotting.Results When 10～8 mol/L Gastrin17 stimulated Colo320WT cells for 12 h,the expression levels of phosphorylated p190RhoGAP increased apparently and RhoA activation diminished.When pAdhFRNK infected Colo320WT cells for 2 d and 10～8 mol/L Gastrin17 treated the cells for 12 h,the expression levels of phosphorylated p190RhoGAP decreased apparently and RhoA activity was elevated.Conclusion hFRNK can inhibit expression of phosphorylated p190RhoGAP and enhanced RhoA activity in the cells stimulated with Gastrin17,and its mechanism is probably that hFRNK can block FAK phosphorylation and FAK pathway.

Objective This study was designed to investigate the relationship between COX-2 and VEGF-C in human gastric carcinomas and discuss the significance of COX-2、VEGF-C in lymph mode metastasis.Methods Forty-two gastric carcinoma tissues and twenty adjacent noncancerous specimens were obtained from surgical resections.COX-2,VEGF-C protein expression was evaluated by immunohistochemical analysis.Results (1)COX-2 was overexpressed in 25 of 42 carcinoma tissues (59.5%) and VEGF-C was 27 of 42(64.3%),which were significantly higher than those in noncancerous tissues (P0.05).(3)There was positive correlation between the expression of COX-2 and VEGF-C(r=0.425,P

To study the effect and mechanisms of 18 α-glycyrrhizic acid (18 α-GA) on cytochrome P450 (CYP) enzymes, the expression of CYP1A1, CYP2E1 and CYP3A was determined in rat hepatocyte sandwich cultures by using enzyme assay and semi-quantitative reverse transcriptase-polymerase chain reaction(RT-PCR). The results showed that the activities of CYP1A1 (7-ethoxyresorufin O-deethylase, EROD), CYP2E1(aniline hydroxylase, ANH) and CYP3A (erythromycin N-demethylase, ERD) were decreased in concentration-dependent manner after treatment with 18 α-GA(50－400 mg*L-1), and at the concentration of 200 mg*L-1 inhibitory rate reached the maximum (the maximum inhibitory rate was 59.6%, 69.7% and 44.7%, respectively). The time course revealed that the inhibition reached plateau level at d 4 of culure. 18 α-GA Decreased CYP1A1, CYP2E1 and CYP3A1 mRNA expression in dose-dependent manner, the maximum inhibitory rate was 44.5% , 58.1% and 37.1%, respectively. The results suggest that 18 α-GA down-regulate CYP expression at the transcriptive levels.