Effect of L-cysteine on colonic motility and the underlying mechanism / 生理学报

The purpose of the present study is to investigate the effect of L-cysteine on colonic motility and the underlying mechanism. Immunohistochemical staining and Western blot were used to detect the localization of the HS-generating enzymes cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE). Organ bath system was used to observe the muscle contractile activities. Whole-cell patch-clamp technique was applied to record ionic channels currents in colonic smooth muscle cells. The results showed that both CBS and CSE were localized in mucosa, longitudinal and circular muscle and enteric neurons. L-cysteine had a dual effect on colonic contraction, and the excitatory effect was blocked by pretreatment with CBS inhibitor aminooxyacetate acid (AOAA) and CSE inhibitor propargylglycine (PAG); L-cysteine concentration-dependently inhibited L-type calcium channel current (I) without changing the characteristic of L-type calcium channel (P < 0.01); In contrast, the exogenous HS donor NaHS increased I at concentration of 100 μmol/L, but inhibited I and modified the channel characteristics at concentration of 300 μmol/L (P < 0.05); Furthermore, L-cysteine had no effect on large conductance calcium channel current (I), but NaHS significantly inhibited I (P < 0.05). These results suggest that L-cysteine has a potential dual effect on colonic smooth muscle and the inhibitory effect might be directly mediated by L-type calcium channel while the excitatory effect might be mediated by endogenous HS.

IL-6 inhibits colonic longitudinal muscle contraction by inactivating L-type calcium channel in rats with pancreatitis / 生理学报

The aim of this study was to investigate the effect of interleukin 6 (IL-6) on the contraction of colon longitudinal muscle strips in rats with acute pancreatitis (AP) and its underlying mechanism. Rat AP model was established by combined injection (i. p.) of ceruletide and lipopolysaccharide. The effect of IL-6 on spontaneous contraction of longitudinal smooth muscle strips of rat colon was observed by biological function experiment system. The level of serum IL-6 was detected by ELISA, the expression and distribution of IL-6 in colon were observed by histochemical staining, and the effect of IL-6 on L-type calcium channel in colon smooth muscle cells was observed by whole cell patch clamp technique. The results showed that, compared with the control group, AP group exhibited reduced contractile amplitude and longer contraction cycle of colon smooth muscle strips. IL-6 prolonged the contraction cycle of colon smooth muscle strips, but did not affect their spontaneous contraction amplitude. Serum IL-6 concentration in AP group was significantly higher than that in control group (P > 0.05). IL-6 was diffusely distributed in the colon of the control group, but the expression of IL-6 was significantly up-regulated in the colon gland, mucosa and submucosa of the AP group. IL-6 significantly decreased the peak current density of L-type calcium channel in rat colon smooth muscle cells. These results suggest that the colon motility of AP rats is weakened, and the mechanism may be that up-regulated IL-6 inactivates L-type voltage-dependent calcium channels, and then inhibits the contraction of colon longitudinal smooth muscle.

Tryptase and Protease-Activated Receptor 2 Expression Levels in Irritable Bowel Syndrome

BACKGROUND/AIMS: Previous studies have revealed that mast cells (MCs) may activate the protease-activated receptors and release of neuropeptides involved in the pathogenesis of irritable bowel syndrome (IBS). The levels of protease-activated receptor 2 (PAR-2) and tryptase can contribute to understanding the pathogenesis of IBS. METHODS: Colonoscopic biopsies were performed of 38 subjects (20 with IBS-diarrhea [IBS-D], eight with IBS-constipation [IBS-C], and 10 healthy volunteers). The mRNA and protein levels of tryptase and PAR-2 were assessed by real-time PCR and Western blot. The levels of vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) were measured by immunohistochemistry, and MCs were counted by toluidine blue staining. RESULTS: Significant increases in the mRNA expression of tryptase (p<0.05, IBS-D, IBS-C vs control) and PAR-2 (p<0.05, IBS-D, IBS-C vs control) and in the tryptase protein level (p<0.05, IBS-D, IBS-C vs control) were detected in IBS. Elevations of MCs, CGRP, VIP and SP (p<0.05, IBS-D vs control) were observed for IBS-D only. CONCLUSIONS: Tryptase levels may upregulate the function of PAR-2, resulting in the release of neuropeptide and they were correlated with clinical symptoms associated with IBS.

Actions of endogenous hydrogen sulfide on colonic hypermotility in a rat model of chronic stress / 生理学报

The present study was designed to investigate the potential role of endogenous hydrogen sulfide (H2S) in chronic stress-induced colonic hypermotility. Male Wistar rats were submitted daily to 1 h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. The total number of fecal pellets was counted at the end of each 1 h of WAS or SWAS session. Organ bath recordings were used to test the colonic motility. H₂S production of colon was determined, and immunohistochemistry and Western blot were performed on rat colonic samples to detect the distribution and expression of H₂S-producing enzymes. The results showed that i) repeated WAS increased the number of fecal pellets per hour and the area under the curve (AUC) of the spontaneous contractions of colonic strips (P < 0.05), ii) repeated WAS decreased the endogenous production of H₂S and the expression of H₂S-producing enzymes in the colon devoid of mucosa and submucosa (P < 0.001), iii) cystathionine-γ-lyase (CSE) was strongly expressed in the cytosols of the circular and longitudinal smooth muscle cells and the nucleus of the myenteric plexus neurons, iv) cystathionine-β-synthase (CBS) was primarily localized in the cytosols of myenteric plexus neurons and weakly localized in the epithelial cells and v) inhibitors of H₂S-producing enzymes increased the contractile activity of colonic strips in the SWAS rats (P < 0.001). In conclusion, the results suggest that the colonic hypermotility induced by repeated WAS may be associated with the decreased production of endogenous H2S.

Diagnosis of obscure gastrointestinal bleeding among different age groups by double balloon enteroscope / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the diagnostic value of double balloon enteroscope (DBE) on obscure gastrointestinal bleeding(OGIB) and to analyze etiological characteristics among different age groups.</p><p><b>METHODS</b>The clinical data of patients undergoing DBE due to OGIB in the Department of Gastroenterology in Renmin Hospital of Wuhan University from January 2007 to January 2012 were retrospectively analyzed and compared among different age groups. Patients were divided into the young group(age≤40, n=86), the middle age group(aged 41-59, n=81), and the elderly group (age≥60, n=49). The detection of bleeding origin by DBE was compared between different age groups.</p><p><b>RESULTS</b>Diagnosis rates in young, middle age, elderly group were 83.7%(72/86), 87.7%(71/81), 81.6%(40/49) without statistical differences(P>0.05). Complication rates in the young, middle age, and elderly group were 1.2%(1/86), 2.5%(2/81), 2.0%(1/49) without statistic difference(P>0.05). The most common cause in young group was diverticulum/replica malformation while the most common location was ileum. The most common cause in both middle age and elderly group was tumor.</p><p><b>CONCLUSIONS</b>DBE is an effective and safe method for diagnosis of OGIB among different age groups. Each age group has its etiological characteristics. Diagnosis and therapeutic strategy based on age-related characteristics is worthy of further investigation.</p>

Aspartate-ornithine granules in the treatment of nonalcoholic steatohepatitis: a multiple-dose parallel controlled clinical trial / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the therapeutic efficacy and safety of aspartate-ornithine granules in patients with nonalcoholic steatohepatitis (NASH).</p><p><b>METHODS</b>Seventy-two patients with NASH were included in this multiple-dose parallel controlled clinical trial and received a 12-week course of aspartate-ornithine granule treatment at either high-dose (6 g bid po; n = 38) or low-dose (3 g bid po; n = 34). Clinical efficacy was assessed by monitoring data from urinalysis, serologic tests (alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and triglyceride (TG)), and abdominal computed tomography (CT) scan. Safety was assessed by occurrence of adverse events (fatigue, anorexia, abdominal distension, nausea, and vomiting). Statistical analyses were conducted to determine the significance of differences between parameters before (baseline) and after treatment.</p><p><b>RESULTS</b>After 12 weeks of treatment, the liver and spleen CT ratios in both the high-dose group (0.89 +/- 0.19) and the low-dose group (0.80 +/- 0.15) were significantly higher than at baseline (S = 329, P less than 0.0001 and S = 246, P less than 0.0001); the overall improvement was more robust in the high-dose group (52.63%) than in the low-dose group (38.23%) (Z = -2.1042, P less than 0.05). After 6 and 12 weeks of treatment, the serum ALT levels in both the high-dose group and the low-dose group were significantly lower than at baseline (6 weeks: S = 324.5, P less than 0.0001 and S = 223, P less than 0.0001; 12 weeks: S = 370.5, P less than 0.0001 and S = 297.5, P less than 0.0001); the overall improvement was more robust in the high-dose group (79.0%) than in the low-dose group (53.0%) (Z = -2.0533, P less than 0.05). Similar trends were seen for the serum levels of AST and GGT after 6 and 12 weeks of treatment (all P less than 0.01) and serum levels of TG after 12 weeks of treatment. The rate of adverse reactions was low and similar between the two groups (high-dose: 4.8% and low-dose: 4.4%; all gastrointestinal).</p><p><b>CONCLUSION</b>Aspartate-ornithine granule therapy was an effective and safe treatment of nonalcoholic steatohepatitis, with the higher dose of 6 g bid po providing more robust clinical benefit without affecting the safety profile.</p>

Impact of PI3K /Akt /mdm2 signaling pathway on the sensitivity of gastric cancer cell line SGC7901 to doxorubicin / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To explore whether PI3K/Akt/mdm2 signalling pathway affect the sensitivity of gastric cancer cell line SGC7901 cells to doxorubicin.</p><p><b>METHODS</b>Gastric cancer cell line SGC7901 cells were exposed to doxorubicin and specific PI3K inhibitor wortmannin. Cell apoptosis was detected using flow cytometry. PI3K activity was detected by radioactive immunoprecipitation-kinase assay. Western blotting was employed to evaluate the expressions of PI3K-p85, pAkt-S473, Akt, pmdm2-S166 and p53.</p><p><b>RESULTS</b>The level of apoptosis in gastric cancer SGC7901 cells treated with doxorubicin was gradually increasing. wortmannin enhanced its effects significantly. PI3K activity and the expression of pAkt-S473 increased in a time-dependent manner, pmdm2-S166, p53 were also increased wortmannin inhibited phosphorylation of mdm2 and improved the p53 expression.</p><p><b>CONCLUSION</b>PI3K/Akt/mdm2 signalling pathway can be activated by doxorubicin and suppress apoptosis by promoting phosphorylation of mdm2. PI3K inhibitor wortmannin can enhance sensitivity of gastric cancer cells to chemotherapy.</p>

The role of p38 MAPK in gastrin-induced u-PA expression in human colon cancer cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the effect of gastrin on the mRNA and protein expression of urokinase-type plasminogen activator (u-PA) in human colon cancer cells and detect the role of p38 MAPK in this process.</p><p><b>METHODS</b>Lipofectin method was used to transfect pCR3. 1/CCK2R vector expressing gastrin receptor into a colon cancer cell line colo320. Gastrin and gastrin antagonist were used to up-regulate and down-regulate the signaling pathway, respectively. Human colon cancer colo320 cells and colo320/ CCK2,R cells were cultured and then stimulated with gastrin for different time; SB203580 was added into culture medium to prevent p38 kinase pathway before incubating with gastrin; Western blot and RT-PCR were used to examine the u-PA expression. Western blot was employed to detect p38 kinase phosphorylation.</p><p><b>RESULTS</b>Gastrin increased evidently the mRNA and protein expressions of u-PA and induced p38 kinase phosphorylation in colo320/CCK,R cells time-dependently. However, the extent of enhancement of u-PA and p38 MAPK expression in colo320 cells was much less than that in colo320/CCK2R cells. The gastrin antagonist L-365, 260 showed an effect of competitive inhibition on gastrin-induced u-PA expression and p38 kinase phosphorylation. The inhibitor SB203580 could sufficiently suppress gastrin-induced p38 kinase phosphorylation and significantly attenuate gastrin-induced u-PA mRNA and protein expressions in colo320/ CCK2 R cells in a dose-dependent manner.</p><p><b>CONCLUSION</b>Gastrin-gastrin receptor signal transduction pathway can obviously induce u-PA expression in human colon cancer cells via activating the phosphorylation of p38 kinase.</p>

Effects of hFRNK on E-cadherin/beta-catenin in colon cancer cells in vitro / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To explore the effects of human FRNK gene on E-cadherin/beta-catenin complex in colon cancer cell line Colo320WT cells stimulated with extrinsic gastrinl7.</p><p><b>METHODS</b>AdEasy system 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 colon cancer cell line Colo320 cells by Lipofectamine 2000 and expressing stably CCK-2R clones were screened by G418 (500 pg/ml). The expression levels of gastrin receptor in Colo320 cells and the transfected Colo320WT cells were assayed by RT-PCR. Colo320WT cells were treated by 10(-8) mol/L gastrinl7 for 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 E-cadherin and beta-catenin in TX-100 soluble fraction and TX-100 insoluble fraction of Colo320WT cells were assayed by co-immunoprecipation and Western blot. E-cadherin and beta-catenin's distribution in Colo320WT cells were detected by immunocytochemistry.</p><p><b>RESULTS</b>When 10(-8) mol/L gastrin17 stimulated Colo320WT cells for 12 h, the expression levels of E-cadherin and beta-catenin in TX-100-soluble fraction decreased apparently, while the expression levels of E-cadherin and beta-catenin in TX-100-insoluble fraction increased markedly. When pAdhFRNK infected Colo320WT cells for 2 d and 10(-8) mol/L gastrin17 treated the cells for 12 h, the expression levels of E-cadherin and beta-catenin in TX-100-soluble fraction increased apparently again, and the expression levels of E-cadherin and beta-catenin in TX-100-insolutble fraction decreased markedly. Immunocytochemistry showed that the distribution of E-cadherin and beta-catenin was translocated from plasma membrane into cytoplasm and nucleus in the cells stimulated with gastrinl7, and after the cells were infected with pAdhFRNK and stimulated by gastrinl7 again. beta-catenin was mainly observed in cytoplasm and little nuclear immunoreactivity.</p><p><b>CONCLUSION</b>An adenovirus vector pAdhFRNK can inhibit abnormal distribution of E-cadherin and beta-catenin in the gastrin17-stimulated cells. The mechanism is probably that hFRNK can disphosphorylate phosphorylated FAK and block FAK pathway.</p>

Reversal of chemoresistance to vincristine in gastric cancer cells by NF-kappaB inhibitor / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the reversing effect of NF-kappaB inhibitor MG-132 on chemoresistance of gastric cancer cells to vincristine.</p><p><b>METHODS</b>In vincristine-resistant human gastric cancer cells (SGC7901/VCR) and the parental sensitive clone (SGC7901), NF-kappaB-DNA binding activity was determined by electrophoreses mobility shift assay (EMSA). The inhibition level of kappaB (IkappaB-alpha) expression was measured by cellular-ELISA. Immunocytochemistry was used to detect the translocation of p65 and chemosensitivity of the cells was determined by MTT assay.</p><p><b>RESULTS</b>Compared with the parental SGC7901 cells, both the baseline and VCR-induced NF-kappaB-DNA binding activities in various concentrations were all higher in the SGC7901/VCR cells. Pretreatment with MG-132, the NF-kappaB inhibitor, for 30 minutes remarkably reduced the NF-kappaB activation, IkappaB-alpha degradation and nuclear translocation of p65. As to the SGC7901/VCR cells and the parental sensitive SGC7901 cells, the IC(50) values for VCR were 40.03 mg/L and 0.26 mg/L, respectively. MG-132 (2.5 micromol/L) significantly enhanced the toxicity of VCR in SGC7901/VCR cells and decreased the resistance index from 154.0 to 16.5. However, MG-132 did not show an obvious effect on the VCR sensitivity in sensitive SGC7901 cells.</p><p><b>CONCLUSION</b>Our data indicate that inhibition of NF-kappaB activation in gastric cancer cells may reverse the drug resistance to VCR in the cancer cells and increase the efficiency of chemotherapy.</p>

Effect of gastrin on invasiveness of human colon cancer cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the effect of gastrin on invasiveness of human colon cancer cells and the role of gastrin receptor-focal adhesion kinase (FAK) signal transduction pathway in this proess.</p><p><b>METHODS</b>pCR3.1/GR vector expressing gastrin receptor was transfected into a colorectal cancer cell line Colo320 with lipofectamine 2000, and screened by G418. The expression levels of gastrin receptor of the parental cell line Colo320 and the transfected cell line Colo320/GR were assayed by RT-PCR. On the other hand, antisense oligonucleotide of FAK was used to block its expression. The mock transfected Colo320 and sense oligonucleotide Colo320 cells were used as controls. Colo320 and Colo320/GR cells were treated with increasing doses (0 approximately 100 nmol/L) of gastrin. Invasiveness of Colo320 and Colo320/GR cells was determined by Boyden chamber. Phosphorylation of focal adhesion kinase (FAK) tyr-397 was examined by immunoprecipitation and Western-blot.</p><p><b>RESULTS</b>RT-PCR results showed that the Colo320/GR cells had an mRNA level four times as high as that of Colo320 cells. Western blot showed that FAK tyr397 phosphorylation of Colo320 cells was apparently decreased. Colo320 and Colo320/GR cells showed a dose-dependent response to gastrin on invasiveness and phosphorylation of FAK tyr-397. Invasiveness of Colo320 cells reached its climax when concentration of gastrin was 100 nmol/L, and FAK tyr-397 phosphorylation was marked when concentration of gastrin was 10 nmol/L, but the latter decreased when gastrin concentration was increased to 100 nmol/L. Colo320/GR cells had the same tendency as Colo320 cells, but showed an even stronger invasiveness and a higher level of FAK tyr-397 phosphorylation than Colo320 cells. Before gastrin stimulation, the invasiveness of Colo320 cells transfected with antisense oligonucleotides and the controls showed no difference. After gastrin stimulation, the increase in invasiveness was much less than that in the controls.</p><p><b>CONCLUSION</b>Gastrin can evidently promote invasiveness of Colo320 cells via gastrin-gastrin receptor-FAK signal transduction pathway.</p>

Effects of nuclear factor kappaB and transforming growth factor beta1 in the anti-liver fibrosis process using Ginkgo biloba extract / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To evaluate the effects of Ginkgo biloba extract (EGB) on CCl(4)-induced liver fibrosis and to investigate the underlying mechanisms.</p><p><b>METHODS</b>Rats were divided into the following groups: normal control group, CCl(4) model group, low dose EGB group, moderate dose EGB group and high dose EGB group. The rat liver fibrosis model was induced by intraperitoneal injection of CCl(4) twice a week for 8 weeks. The model rats of the three EGB treated groups were given 0.25 g/kg, 0.5 g/kg, 1.0 g/kg of EGB by stomach tubes every day. At the end of the eighth week, the blood and liver specimens were obtained. The expressions of nuclear factor kappaB (NF-kappaB) P65, and alpha-smooth muscle actin (alpha-SMA) were detected by immunohistochemistry. Radioimmunoassay was exploited to evaluate serum hyaluronic acid (HA) and laminin (LN) levels. Electrophoretic mobility shift assay (EMSA) was used to confirm the nuclear translocation activity of NF-kappaB in liver tissues. The mRNA expression of transforming growth factor-beta1 (TGFbeta1) and collagen I was determined by RT-PCR. Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver tissues and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the sera were also examined.</p><p><b>RESULTS</b>CCl(4) administration induced liver fibrosis, which was inhibited by EGB in a dose-dependent manner. The histopathologic scores of liver fibrosis, the levels of serum ALT, AST, HA and LN were significantly lower in the rats treated with EGB compared with those not treated (P <0.01 or P <0.05). SOD and GSH-Px activities were notably elevated and MDA content was significantly lower in the rats treated with EGB (P <0.01 or P <0.05), indicating reduced oxidative stress. Immunohistochemical staining demonstrated inhibition of hepatic stellate cell (HSC) activation (in terms of alpha-SMA expression) and NF-kappaB P65 expression in the livers of the EGB-treated rats. As determined by EMSA and RT-PCR, activation of NF-kappaB, the mRNA expression of TGFbeta1 and collagen I were significantly higher in model group rats, but obviously lower in EGB treated rats.</p><p><b>CONCLUSION</b>EGB is able to ameliorate liver injury and prevent rats from CCl(4)-induced liver fibrosis by suppressing oxidative stress. This process may be related to inhibiting the expression of TGFbeta1 and the induction of NF-kappaB on HSC activation.</p>

Relationship between alterations of p16INK4a and p14ARF genes of CDKN2A locus and gastric carcinogenesis / 中华流行病学杂志

<p><b>OBJECTIVE</b>To investigate the relationship between alterations of p16INK4a and p14ARF genes and gastric carcinogenesis.</p><p><b>METHODS</b>Tumors and gastric tissues neighboring carcinoma from 48 patients with gastric cancer were studied. Homozygous deletion, mutation, methylation of the CpG islands, mRNA expression of p16INK4a and p14ARF genes were assessed by polymerase chain reaction (PCR), PCR-single strand conformation polymorphism (SSCP), PCR based methylation assay, and reverse transcription (RT)-PCR.</p><p><b>RESULTS</b>(1) The overall homozygous deletion rate of p16INK4a and p14ARF was 35.4% (17/48), and no homozygous deletion was examined in all the gastric tissues neighboring tumor. (2) There was no point mutation of p16INK4a and p14ARF in 31 gastric cancers without homozygous deletion and in the matched gastric tissues adjacent to tumor. (3) Methylation of the CpG islands of p16INK4a and p14ARF was detected in 47.9% (23/48) of gastric cancers, while methylation was observed only in 2 of 48 gastric tissues neighboring cancers with a significant difference (P <0.01). (4) The rate of p16INK4a mRNA loss was 47.9% (23/48) in gastric cancer, and the cases of combined methylation of exons 1alpha and 2 had a higher loss rate (100%, 6/6) of p16INK4a mRNA than those of methylation form the other exons (11.8%, 2/17) (P <0.01). The loss rate of p14ARF mRNA was 45.8% (22/48) in gastric cancer, and patients with combined methylation of exons 1beta and 2 had a higher loss rate (100%, 3/3) of p14ARF mRNA than those of the methylation from the other exons (15%, 3/20) (P < 0.05). (5) The combined loss of p16INK4a and p14ARF mRNAs was examined in 1 (5.6%) of 18 cases of well and moderately-differentiated carcinomas, and 11 (36.7%) of 30 cases of poorly and not-differentiated carcinomas with significant difference (P <0.05).</p><p><b>CONCLUSION</b>p16INK4a and p14ARF genes were frequently inactivated by homozygous deletion and methylation of the 5' CpG islands in gastric cancer, which might have played an important role in the development of gastric cancer.</p>

Nimesulide, a selective cyclooxygenase-2 inhibitor inhibits telomerase activity by blocking activation of PKB in gastric cancer cell line / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the effects of nimesulide, a selective COX-2 inhibitor, on cell viability, telomerase and PKB activities in human gastric cancer cell line SGC7901 and to explore its molecular mechanism of selective growth inhibition.</p><p><b>METHODS</b>MTT assay was used to determine cell viability after incubation for 0, 12, 24, and 48 h in different concentrations (0, 25, 50, 100, 200 micro mol/L) of nimesulide and/or okadaic acid (300 nmol/L). Telomerase and protein kinase B (PKB) activities were detected using TRAP PCR-ELISA and nonradioactive IP-kinase assay.</p><p><b>RESULTS</b>Nimsulide caused a time and dose-dependent reduction of cell numbers of SGC7901. The telomerase and PKB activities were significantly inhibited, and the inhibition of telomerase activity was partly associated with decrease in PKB activity.</p><p><b>CONCLUSION</b>Selective COX-2 inhibitor nimesulide inhibits telomerase activity of gastric cancer cells by partly blocking the activation of protein kinase B. The results suggest an additional signaling pathway underlying the anti-cancer effect of COX-2 inhibitor.</p>

Effects of bererine on basolateral potassium current of rat colonic crypt cells / 中华消化杂志

Objective To investigate the effects of berberine on basolateral calcium-activated potassium current I_K(Ca)and cAMP-activated potassium current I_K(cAMP)and its mechanism in treatment of secretory diarrhea.Methods The intact colonic crypt cells were isolated with EDTA solution.The effects of berberine(50,100,500?mol/L)on I_K(Ca)and I_K(cAMP)were detected by patch clamp technique under the conventional whole cell patch clamp mode.The solution of PSS was served as control.Results Berberine could significantly inhibite I_K(Ca)and I_K(cAMP)of rat colonic crypt cells(both P

Comparisons of endoscopic and pathological characteristics between long and short segment Barrett's esophagus / 中华消化杂志

Objective To investigate the similarities and differences of endoscopic and pathological char- acteristics between long and short segment Barrett's esophagus.Methods One hundred and twenty-eight cases of Barrett's esophagus identified both by endoscopy and pathology were enrolled in this retrospective study. Among them,40 cases were long segment Barrett's esophagus (LSBE) and 88 were short segment Barrett's esophagus (SSBE).The age distribution,sex distinction,endoscopic manifestations and pathological changes were assessed.Data were statistically analyzed by t-test or u-test.Results There were no differences in age distribution and sex distinction between LSBE and SSBE groups (P＞0.05).The ring pattern was the most prominent type accounting for 62.5% in LSBE group.The island pattern was the most prominent type accounting for 85.2% in SSBE group.There were significant differences in the rates of specialized intestinal metaplasia between LSBE and SSBE groups(47.5% vs 14.8%,P＜0.01).Moreover,among the special- ized intestinal metaplasia,low grade (15.0% vs 4.5%),medium grade (12.5% vs 3.4%) and high grade dysplasia (5.0% vs 0.0%) between LSBE and SSBE groups also had statistical differences (all P＜0.05).Conclusions LSBE may have more tendency in dysplasia than that of SSBE.We should pay attention to the importance of endoscopic manifestations and pathological diagnosis.