Therapeutic value of endoscopic submucosal dissection for early stage colorectal cancer and precancerous lesions / 中华消化内镜杂志

Objective To investigate the safety and efficacy of endoscopic submucosal dissection ( ESD) for early stage colorectal cancer and precancerous lesions. Methods Clinical data of 108 patients who received ESD for early stage colorectal cancer and precancerous lesions from December 2016 to June 2017 in Renmin Hospital of Wuhan University were analyzed. The lesion characteristics, postoperative pathological features, intraoperative and postoperative complications and postoperative follow-up outcomes were analyzed. Results The 108 patients all underwent ESD successfully with median operation time of 45 min. The rate of intraoperative perforation and postoperative delayed bleeding was 2. 8％ ( 3/108) and 2. 8％ (3/108), respectively. No postoperative delayed perforation occurred. Postoperative pathology showed that there were 41 cases ( 38. 0％) of tubular adenoma, 4 ( 3. 7％) villous adenoma, 39 ( 36. 1％) villous tubular adenoma [ including 41 ( 38. 0％) low-grade intraepithelial neoplasia and 16 ( 14. 8％) high-grade intraepithelial neoplasia] , 19 ( 17. 6％) adenocarcinoma, and 5 ( 4. 6％) other types. Among the 19 cases of adenocarcinoma, there were 11 cases of well-differentiated, 5 median-differentiated and 3 low-differentiated. The complete resection rate was 100. 0％ and the en bloc resection rate was 92. 3％ ( 100/108) . The mean follow-up time was 8. 1 months, and no recurrence was found during this period. Conclusion ESD is safe and effective in the treatment of early stage colorectal lesions. It is important to improve preoperative assessment, strengthen surgical skills, analyze postoperative pathological features and regularly follow up to guarantee the treatment quality of ESD.

Endoscopic submucosal dissection for colorectal lesions in elderly patients / 中华消化内镜杂志

Objective To investigate the safety and effectiveness of endoscopic submucosal dissection(ESD)for elderly patients(≥60 years old)with colorectal lesions.Methods Data of 31 elderly patients(≥60 years old)and 23 non-elderly(0.05 ). Thirty-two lesions in elderly group and twenty-five lesions in non-elderly group were all curative resection.En bloc resection rates were 96.9%(31 /32)and 96.0%(24 /25)in the elderly group and non-elderly group respectively;the rates of bleeding during ESD procedure were 3.2%(1 /31 )and 4.3%(1 /23);delayed bleeding rates were 12.9%(4 /31)and 13.0%(3 /23);the rates of perforation was 12.9%(4 /31)and 0;postoperative infection rates were 3.2%(1 /31)and 4.3%(1 /23)respectively.There were no statistical differences between the two groups in any of these data (P >0.05 ).The mean time of follow-up were (14.8 ±1.7)months in elderly group and (14.7 ±1.8)months in non-elderly group,and there was no significant difference between two groups.No residual lesion or recurrent lesion was found in the follow-up period.Conclusion ESD is a safe and effective treatment for the elderly patients with colorectal lesion.

Fuji intelligent chromo endoscopy for the diagnosis of Barrett esophagus / 中华消化内镜杂志

ObjectiveTo evaluate the Fuji intelligent chromo endoscopy (FICE) in the diagnosis of Barrett esophagus (BE).MethodsFrom September 2010 to March 2011,a total of 180 patients with suspected reflux esophagitis were examined successively by FICE,magnifying FICE,acetic dyeing endoscopy and magnifying acetic dyeing endoscopy.The diagnosis was made out under the observation of lesion extensions,superficial mucosa contrast ratio,pit patterns and capillary forms of BE.The endoscopic diagnosis was made and compared with the pathologic diagnosis,and the consistency of the diagnosis was evaluated by Kappa value.ResultsBE was confirmed in 35 patients ( 19.4％ ) pathologically.The consistency rates of diagnosis under FICE and acetic dyeing endoscopy were 81.7％ and 72.8％ ( P ＜ 0.05 ).The consistency rates of diagnosis under magnifying FICE and magnifying acetic dyeing endoscopy were 97.8％ and 85.6％,respectively (P ＜ 0.05).FICE magnifying endoscopy revealed better mucosal structures of capillaries than magnifying acetic dyeing endoscopy did ( P ＜ 0.05 ),but there was no significant difference in revealing of duct openings (P ＞ 0.05).The specificity,sensitivity,positive predictive value,negative predictive value and Kappa value of FICE in diagnosis of BE were 82.1％,80.0％,51.9％,94.4％ and 0.52,respectively,which were 73.2％,71.4％,39.1％,91.4％ and 0.34 of acetic dyeing endoscopy,98.6％,94.3％,94.3％,98.6％ and 0.93 of magnifying FICE,and 88.3％,74.3％,60.5％,93.4％ and 0.58 for magnifying acetic dyeing endoscopy.ConclusionAs a neotypical endoscopic system,magnifying FICE could exhibit clearly the pit patterns and microvascular structures of esophagus mucosa,and it can capture the optimal images of Barrett's epithelium.FICE could improve the diagnosis of BE in vivo.

Fuji intelligent color enhancement chromoendoscopy for diagnosis of early gastric cancer / 中华消化内镜杂志

ObjectiveTo evaluate Fuji intelligent color enhancement (FICE) chromoendoscopy for diagnosis of early gastric cancer. MethodsFrom February 2010 to March 2011 ,a total of 67 patients with suspected gastric mucosal lesions were enrolled in this study. The lesions were observed with magnifying endoscopy, FICE, magnifying chromoendoscopy and indigo-carmine-magnifying-chromoendoscopy.Suspected gastric mucosal pit patterns and microvascular morphology were compared. Targeted biopsy was performed on suspected locations. Sensitivity, specificity and pathological consistency were compared between the 3 procedures. ResultsOut of 67 patients, 17 were diagnosed as having early gastric cancer.There was no difference among magnifying endoscopy, FICE magnifying chromoendoscopy and indigo-carmine-magnifying-chromoendoscopy in pit pattern findings,however, FICE magnifying chromoendoscopy was superior to other 2 procedures in displaying capillary loop. The sensibility, specificity and pathological accordance rate of FICE magnifying chromoendoscopy were 94. 1％ ( 16/17 ), 98. 0％ (49/50) and 97.0％(65/67), which were higher than those of the magnifying endoscopy [58.8％ ( 10/17), 84％ (42/50)and 77.6％ ( 52/67 )] ( P ＜ 0. 05 ), and were not different from those of indigo-carmine-magnifying-chromoendoscopy [88.2％ (15/17), 96％ (48/50) and 94.0％ (63/67)] (P ＞0.05). Conclusion FICE magnifying chromoendoscopy provides rather clear images of gastric mucosa and intrapapillary capillary, thereby improving the accuracy of endoscopic biopsy and then imporving the diagnosis rate of early gastric cancer.

The impact of Akt and nuclear factor κB pathway on chemoresistance of gastric cancer cell / 中华消化杂志

Objective To evaluate the role of Akt and nuclear factor (NF)-κB pathway in the development of chemoresistance in gastric cancer and the relation between Akt and NF-κB.Methods SGC-7901 cells were exposed to chemotherapeutic drugs (doxorubicin and etoposide ) or chemotherapeutic drugs combined with Wortmannin or MG-132.The cell growth was detected using MTT method.The apoptosis of SGC-7901 cells was measured by TUNEL and Annexin V/PI methods.The protein level of NF-κB was analyzed by immunocytochemical staining.Electrophoretic mobility shift assay (EMSA) was used to confirm the increased nuclear translocation of NF-κB/P65.chemotherapeutic drugs could obviously inhibit the growth of SGC-7901 cells in time-dose-dependent manner.Pretreatment of SGC-7901 cells with Wortmannin or MG-132 could promote this inhibitory κB in a dose-dependent manner.Wortmannin or MG-132 pretreatment could enhance the apoptosis of NF-κB was found in SGC-7901 cells stimulated with Wortmannin,but no activation of Akt was noted in those treated with MG-132.Conclusions The chemotherapeutic drugs can both induce apoptosis and activate Akt and NF-κB in SGC-7901 cells.The efficacy of chemotherapeutic drugs can be increased via inhibiting activation of Akt or NF-κB.

Significance and expression of E-cadherin and focal adhesion kinase in rectal cancer / 中华消化外科杂志

Objective To investigate the significance and expression of E-cadherin(E-CD),focal adhesion kinase(FAK)and FAK py397 in rectal cancer.Methods Thirty paraffin specimens of rectal cancer and adjacent tissues collected from 2001 to 2002 and 35 fresh specimens of rectal cancer and adjacent tissues resected from 2006 to 2007 at People's Hospital of Wuhan University were adopted in this study.The expression of E-CD,FAK and FAK py397 was detected by immunohistochemistry and Western blot.All data were analyzed using chi-square test.Results E-CD was positively expressed in the membranes of epithelial cells in normal rectal mucosa,while no E-CD expression was found in the membranes of epithelial cells in rectal cancer tissues.There was a significant correlation between the expression of E-CD,FAK,FAK py397 and tumor difierentiation,depth of invasion and lymph node metastasis(χ~2=7.099,18.358,25.612;12.316,28.823,23.168;8.927,18.122,22.620,P＜0.05),while no relationship between the expression of E-CD,FAK,FAK py397 and age,sex was detected(χ~2=0.439,1.899,3.676;0.541,4.051,1.135,P＞0.05).The expression levels of FAK and FAK py397 were 83% (54/65)and 68% (44/65)in rectal cancer tissues,and were 31%(20/65)and 26% (17/65)in adjacent tissues,with significant difference(χ~2=33.707,34.163,20.897,P＜0.05).Conclusion Lost expression of E.CD in the membrane of rectal cancer tissue and elevated expression of FAK and FAK py397 in the rectal cancer tissue might be related to the invasion and metastasis of rectal cancer,which may predict the biological behavior of rectal cancer.

The expression and role of PTEN in doxorubicin induced gastric cancer cell apoptosis / 中华内科杂志

Objective To study the expression of PTEN and its significance in doxorubicin-treated gastric cancer cells. Methods (1) Gastric cancer BGC-823 cells were treated with doxorubicin. Cell proliferation and apoptosis were evaluated by MTF and flow cytometry. The expression of PTEN at the mRNA and protein level were determined by RT-PCT and Western blot, respectively. (2)The gastric cancer xenografts model was constructed. The apoptosis of gastric cancer xenografts cells was determined by TUNEL. The expression of PTEN at the mRNA and protein level were detected using RT-PCR and Western blot, respectively. (3) BGC-823 cells were transfected with PTEN siRNA before addition of doxorubicin. The proliferation and apoptosis of these cells as well as the expression level of PTEN protein were determined. Results (1) After administration of doxorubicin, the proliferation of BGC-823 cells was inhibited in a time-dependent manner. (2) Doxorubicin significantly induced apoptosis of BGC-823 cells. (3) Doxorubicin treated BGC-823 cells showed a significant increase in the expression of PTEN at the mRNA and protein level in a time-dependent manner. TUNEL assay also showed a significant increase of apoptosis rate in gastric cancer xenografts treated with doxorubicin compared with control group [(28. 11± 1.05) % vs (2. 78 ± 1.63) %]. The expression of PTEN at the mRNA and protein level in the gastric cancer xenografts were significantly increased after administration of doxorobicin (0. 5667 ± 0. 0043 vs 0.2217±0.0063,0.14±0.26 vs 0.04±0.15,P <0.05). (4) After treated with doxorubicin, the expression of PTEN in siRNA-transfected BGC-823 cells was significantly higher than that in non-transfected BGC-823 cells (P < 0. 0001). The apoptosis of PTEN siRNA-transfected BGC-823 cells was significantly decreased compared with non-transfected BGC-823 cells [(10. 35 ± 1.04) % vs (31.37 ± 3.58) %, P < 0. 05]. Conclusion Doxorubicin can effectively inhibit the growth and induce the apoptosis of BGC-823 gastric cancer cells. Increasing PTEN protein may be one of the main mechanism involved in this effect.

24 h esophageal pH monitoring in patients with gastroesophageal reflux-induced cough treated with omeprazole / 中华全科医师杂志

To monitor the 24 h esophageal pH in patients with gastroesophageal reflux-induced cough (GERC) before and after omeprazole treatment. Methods The prospective study was conducted in Department of Gastroenterology, People's Hospital of Wuhan University from February 2007 to April 2008. Twenty patients with GERC received 40 mg of omeprazole daily and underwent 24 h esophageal pH monitoring before and 8 weeks after omeprazole treatment. Six parameters by Johson and Demeester were adopted for evaluation: pereentage of total time with pH <4, percentage of uptight reflux time with pH <4, percentage of supine reflux time with pH < 4, the number of reflux episodes with pH < 4, the number of reflux episodes longer than 5 min and the percentage of longest reflux duration. Results The values of six parameters before treatment were 13.5±8.5, 12.2±4.0, 15.8 ±4.1, 56 ± 13, 4. 15 ± 1.87 and 26.2 ± 16. 5 respectively; while those after treatment were 2.7± 1.3, 3.9 ± 1.9, 1.9 ± 1.0, 18 ± 11, 1.24 ±0.65 and 7.4 ± 2. 1. There were significant differences in these six parameters between pre-treatment and post-treatment (P<0.01 ). Conclusion The 24 h esophageal pH monitoring shows that omeprazole is effective in treatment of GERC by decreasing esophageal pH.

Expression of P57(kip2) and cyslinE proteins in human pancreatic cancer / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of p57(kip2) and cyclinE proteins on the genesis and progression of human pancreatic cancer.</p><p><b>METHODS</b>The expression of p57(kip2) and cyclinE proteins in tumor tissues and adjacent tissues of pancreatic cancer in 32 patients was detected by SP immunohistochemical technique.</p><p><b>RESULTS</b>The p57(kip2) protein positive-expression rate in tumor tissues of pancreatic cancer was 46.9%, which was lower than that in adjacent pancreatic tissue (P < 0.05). The p57(kip2) protein positive-expression correlated significantly with tumor cell differentiation (P < 0.05) and did not correlate significantly with lymph node metastasis (P > 0.05). The cyclinE positive-expression rate in tumor tissues was 68.8%, which was higher than that in adjacent pancreatic tissues (P < 0.05). The cyclinE positive-expression also correlated significantly with tumor cell differentiation and lymph node metastasis (P < 0.05). The cyclinE protein positive-expression rate in the tumor tissues of the p57(kip2) protein positive-expression group was lower than that in the p57(kip2) protein negative-expression group, and there were no significant correlation between the two groups (r = -0.112, P > 0.05).</p><p><b>CONCLUSION</b>Decreased expression of the p57(kip2) protein and/or over-expression of the cyclinE protein may play an important role in the genesis and progression of human pancreatic cancer.</p>

Relationship between alterations of p16(INK4a) and p14(ARF) genes of CDKN2A locus and gastric carcinogenesis / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the relationship between alterations of p16(INK4a) and p14(ARF) genes and gastric carcinogenesis.</p><p><b>METHODS</b>The tumors and neighboring gastric tissues from 48 patients with gastric cancer were studied. The homozygous deletion, mutation, methylation of the CpG islands, and mRNA expression of p16(INK4a) and p14(ARF) genes were assessed by PCR, PCR-SSCP, PCR based methylation assay, and RT-PCR.</p><p><b>RESULTS</b>(1) The homozygous deletion rate of p16(INK4a) and p14(ARF) was 35.4% (17/48), and no homozygous deletion was examined in any gastric tissue neighboring the tumor. (2) There was no point mutation of p16(INK4a) and p14(ARF) in 31 gastric cancers without homozygous deletion or in the matched gastric tissues adjacent to the tumor. (3) Methylation of the CpG islands of p16(INK4a) and p14(ARF) was detected in 47.9% (23/48) of gastric cancers, while methylation was observed only in 2 of 48 gastric tissues neighboring the cancer with a significant difference (P < 0.01). (4) The loss rate of p16(INK4a) mRNA was 47.9% (23/48) in gastric cancer, and the patients of the combined methylation of exons 1alpha and 2 had a higher loss rate (100%, 6/6) of p16(INK4a) mRNA than those of the methylation of the other exons (11.8%, 2/17, P < 0.01); the loss rate of p14(ARF) mRNA was 45.8% (22/48) in gastric cancer, and patients with the combined methylation of exons 1beta and 2 had a higher loss rate (100%, 3/3) of p14(ARF) mRNA than those of the methylation of the other exons (15%, 3/20, P < 0.05). (5) The combined loss of p16(INK4a) and p14(ARF) mRNAs was examined in 1 (5.6%) of 18 patients of well and moderately-differentiated carcinomas, and 11 (36.7%) of 30 patients of poorly and not-differentiated carcinomas with a significant difference (P < 0.05).</p><p><b>CONCLUSION</b>p16(INK4a) and p14(ARF) genes are frequently inactivated by homozygous deletion and methylation of the 5'CpG islands in gastric cancer, which may play an important role in the carcinogenesis of gastric cancer.</p>

The effects of paeonol on inhibiting the proliferation of human colorectal cancer cell line HT-29 and its molecule mechanism / 中国药理学通报

Aim To investigate the effects of paeonol(Pae)in inhibiting the proliferation of HT-29 cell and probe into the possible molecule mechanism by quantitative and qualitative assay.Methods The inhibited rate and apoptotic rate of HT-29 cells were measured quantitatively by MTT assay.We were trying to find out the possible mechanism through the morphologic observation on paeonol-processed HT-29 cell line by TUNEL assay and immunocytochenical method.Results Pae,in the concentration of 0.024～1.504 ?mol?L~(-1),inhibited the proliferation of HT-29 cells in vitro,which showed obvious concentration-effect relationship;The inhibited rate of HT-29 cells was also increased when Pae(0.024～1.504 ?mol?L~(-1))was treated for 24,48,72 and 96 h,which showed obvious time-effect relationship.After treated with the concentration of 1.504 ?mol?L~(-1),the apoptotic rate of HT-29 cells significantly increased,which showed significant difference compared with control;We examined all the experimental groups by flow cytometry,which showed that sub-G_1 peak appeared before G_1 period and the cells in S period increased,while the cells in G_1、G_2 period decreased,the apoptotic rate of HT-29 cells gradually increased along with the increasing of paeonol concentration.The apoptotic rate in experimental groups vs control has significant difference(P

Effects of adenovirus vector expression hFRNK on phosphorylated 190RhoGAP and RhoA Activity in colo320WT colorectal cells / 中国实用内科杂志

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.

THE EXPRESSION OF CYCLIND1 AND P21WAF1 IN COLORECTAL CARCINOMA / 中国内镜杂志

Objective:To investigate expression of cyclinD1 and p21WAF1 and their relationship with multistage process of colon carcinogenesis.Methods:Immunohistochemical staining was performed with SP assay on archival materials from 40 colorectal carcinomas,28 colorectal adenomas,and 14 normal mucosa,cyclinD1 and p21WAF1 expression were compared.Results:The positive staining rate for cyclinD1 in colorectal adenomas and carcinomas is 92.9% and 67.5% respectively,which are both higher than that in the normal mucosa (35.7%) (Padenoma＜0.01，Pcarcinoma＜0.05) and the expression of cyclinD1 is not correlate with differentiation and lymph node metastasis of colorectal carcinoma.The positive stainimg rate for p21WAF1 in normal mucosa (92.9%) is higher than that in colorectal carcinoma(37.5%) (P＜0.01) and the expression of p21WAF1 is correlate with differentiation and lymph node metastasis of colorectal carcinonma.Conclusions:The aberrant expression of cyclinD1 and p21WAF1 is a common event during multistage process of colon carcinogenesis.

18 α-Glycyrrhizic acid down-regulated the activities and mRNA expression of cytochrome P450 isoenzymes in rat hepatocyte sandwich cultures / 中国药理学与毒理学杂志

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.

EFFECTS OF 18α-GLYCYRRHIZIC ACID ON RAT LIVER CYTOCHROME P450 ISOENZYMES AND PHASE II TRANSFERASE / 药学学报

AIM　To study the effect of 18α-glycyrrhizic acid (18α-GL) on hepatic microsomal drug metabolizing enzymes in rats. METHODS　18α-GL (12.5, 50.0 mg*kg-1*d-1) were given ip to male Wistar rats for 3, 6 or 12 consecutive days. The rats were sacrificed 24 h after the last dose and the liver microsomes were prepared for analysis of cytochrome P450 (CYP) isozymes and phase II transferase activites. RESULTS Aniline hydroxylase (CYP2E1) activities in the rats treated with 18α-GL (12.5, 50.0 mg*kg-1) for 6 days decreased dose-dependently by up to 53.2%; For 3, 6 or 12 days 7-ethoxyresorufin O-deethylase (CYP1A1) activities in the rats of 50 mg*kg-1 dose group decreased time-dependently by 17.6%, 38.3% and 47.3%, respectively; Erythromycin N-demethylase (CYP3A) activities was significantly inhibited from 23.1% to 34.3%. UDP-glucuronosyltransferase activities toward 7-hydroxy-4-methylcoumarin significantly increased ranging from 19.3% to 29.9%. UDP-glucuronosyltransferase activities toward 4-phenylphenol in the rats treated with 18α-GL (12.5, 50.0 mg*kg-1) for 6 days increased by 45.9% and 70.3%. Glutathione S-transferase (GST) activities in the rats treated with 18α-GL (12.5，50.0 mg*kg-1) for 6 days increased by 13.7% and 48.3% in dose-dependent manner. CONCLUSION　18α-GL inhibited rat liver microsomal cytochrome P450 while induced phase II transferase.

Effects of combination of octreotide and wortmannin on proliferation of gastric carcinoma cell BGC-823 / 中国实用内科杂志

Objective To investigate the effect and mechanism of octreotide with or without wortmannin on the growth of gastric carcinoma cell BGC-823.Methods From June to August of 2007,in Remin Hospital of Wuhan University,cells were exposed to octreotide for four dilution(10-5、10-4、10-3、10-2g/L)with or without wortmannin(a special inhibitor of PI3'K/Akt pathway,the dilution is 40 nmol/L).And then the cytotoxicity was assessed by determining cell survival with MTT after 24 hours,with also were exposed to octreotide for the dilution of 10-3 g/L with or without Wortmannin in 12 h,24 h,36 h,48 h,then the cell survivral rate was accounted and the results were formulated in a table,and the cell cycle was checked-out with Flow Cytometer(FCM);the expression level of p27 gene and protein was determinated with RT-PCR and Western-bloting Test.Results The five groups within one reagent treating were compared with control group,and the results had difference,but the combination of two reagents group had significant difference(P

Activity of PI3′K/Akt/FKHRL1 signaling pathway induced by doxorubin confer chemoresistance in gastric cancer cell / 中国实用内科杂志

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.

Effect of ginkgo biloba extract on expression of Activin A in hepatic fibrosis of rat / 中国实用内科杂志

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

Clinical study on endoscopic therapy of giant gastrointestinal lipomas / 中华消化杂志

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 (

Effect of activation of protein kinase B and Caspase-9 signal transduction pathway of human gastric cancer cells on the cell chemosensitivity to etoposide / 中华消化杂志

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.