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Mindin is upregulated during colitis and may activate NF-κB in a TLR-9 mediated manner

World Journal of Gastroenterology 2010年第9期16卷 1070-1075页

作者： bayasi guleng Division of Gastroenterology Zhongshan Hospital Affiliated to Xiamen University

AIM:To investigate the regulation of mindin expression and the signaling pathway involved during ***:C57BL/6 mice were treated with 3% dextran sulfate sodium (DSS) in drinking water for 6 d to induce acute colitis,and then the colon was harvested for histological analysis or for RNA *** expression of mindin and nuclear factor (NF)-κB p65 was analyzed by quantitative real time polymerase chain reaction (RT-PCR) and mindin expression construct was conf irmed by Western *** macrophage and intestinal epithelial lineage cells were stimulated with different cytokines and toll-like receptor (TLR) ligands,before pNF-κB-luciferase activity was assessed using the Dual-Luciferase reporter assay ***:mRNA expression of mindin was upregulated 4.7 ± 1.1 fold compared with the baseline during DSS-induced intestinal inflammation in the *** with CpG-ODN (a known TLR-9 ligand) induced 4.2 ± 0.3 fold upregulation of mindin expression in RAW 264.7 ***-length of mindin was cloned from cDNA of mouse mesenteric lymph node,then the pCMV-Mindin-Flag expression vector was established and the protein expression level was confi *** of the mindin construct and stimulation with CpG-ODN signifi cantly increased the NF-κB-luciferase activity by 2.5 ± 0.3 and 4.5 ± 0.5 fold in RAW264.7 and CMT93 cells,respectively (P < 0.01).CONCLUSION:Mindin expression is upregulated during intestinal inflammation and may induce NF-κB promoter activation in a TLR-9 mediated manner.

关键词： Mindin Nuclear factor-κB promoter activity Toll-like receptor-9

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Cancer-derived VEGF plays no role in malignant ascites formation in the mouse

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World Journal of Gastroenterology 2005年第35期11卷 5455-5459页

作者： bayasi guleng Keisuke Tateishi Fumihiko Kanai Amarsanaa Jazag Miki Ohta Yoshinari Asaoka Hideaki Ijichi Yasuo Tanaka Jun Imamura Tsuneo Ikenoue Yasushi Fukushima Keita-Morikane Makoto Miyagishi Kazunari Taira Takao Kawabe Masao Omata Department of Gastroenterology Graduate School of Medicine University of Tokyo 7-3-1 HongoBunkyo-ku Tokyo 113-8655 Japan Clinical Research Center University of Tokyo Hospital 7-3-1 Hongo Bunkyo-ku Tokyo113-8655 Japan Infectious Disease Surveillance Center NationalInstitute of Infectious Diseases 1-23-1 Toyama Shinjuku-ku Tokyo162-8640 Japan Department of Chemistry andBiotechnology Graduate School of Engineering University of TokyoTokyo 113-8656 Japan

AIM: Vascular endothelial growth factor (VEGF) is a potent mediator of peritoneal fluid accumulation following tumor progression. This study investigated the role of VEGF secreted by cancerous cells in the formation of malignant ***: VEGF expression was eliminated byknockdown in the pancreas cancer cell-line PancO2 using vector-based short-hairpin type RNA interference (RNAi).Malignant ascites formation in the mouse was analyzed by intraperitoneal injection of PancO2 cells expressing VEGF or with expression ***: The VEGF knockdown PancO2 cell was successfully established. Knockdown of VEGF did not affect cancer cell proliferation in vitro or in vivo. The volume of ascites following peritoneal expansion of the tumor in VEGF knockdown cells and control cells did not differ statistically in this in vivo study. Moreover, the VEGF concentration in the ascites did not differ ***: Malignant ascites formation might be mediated by VEGF production in noncancerous tissues,such as stromal compartments. An anti-VEGF strategy against malignant ascites could be applied to various tumors regardless of whether they secrete VEGF.

关键词： VEGF, Ascites RNAi

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β-arrestinl在胃癌细胞BGC-823中的生物学功能

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中华消化杂志 2012年第9期32卷 615-619页

作者：王旭王璐董菁巴亚斯古楞任建林厦门大学附属中山医院消化科 361004

目的探讨β-arrestinl对胃癌细胞BGC-823增殖、迁移、侵袭及凋亡能力的影响。方法用实时定量PCR技术及Western印迹法检测人胃黏膜上皮细胞GES和人胃癌细胞株BGC-823、MKN-28、SGC-7901中parrestinl的表达水平。应用RNA干扰技术构建稳定... 详细信息

目的探讨β-arrestinl对胃癌细胞BGC-823增殖、迁移、侵袭及凋亡能力的影响。方法用实时定量PCR技术及Western印迹法检测人胃黏膜上皮细胞GES和人胃癌细胞株BGC-823、MKN-28、SGC-7901中parrestinl的表达水平。应用RNA干扰技术构建稳定干扰β-arrestinl和阴性对照组（pU6空载体）的BGC-823细胞株。进一步应用细胞计数法、划痕实验、Transwell小室实验及流式细胞术分析干扰β-arrestinl和阴性对照组的BGC-823细胞株的增殖、迁移、侵袭能力及凋亡水平的变化。统计学处理采用t检验。结果β-arrestinl在GES表达量为0．001士0．001，MKN-28表达量为0．002±0．000，SGC-7901表达量为0．003±0．002，BGC-823中表达量为0．005±0．000。干扰3-arrestinl和阴性对照的BGC-823细胞增殖抑制率分别为-30．2％和100．0％，迁移能力受到抑制，穿过基质膜细胞数分别为126．25±3．24和213．50±6．27（t=0．000，P〈O．01），凋亡率为（41．350±1．053）％和（11．497±0．589）％（t=0．015，P〈0．05）。结论β—arrestinl在胃癌细胞中高水平表达，并且随着胃癌细胞恶性度增高而表达量增加，在BGC-823细胞中干扰parrestinl后能抑制细胞的生长、迁移、侵袭，并提高凋亡水平。

关键词： β-arrestin1 胃肿瘤 RNA干扰肿瘤细胞培养的

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Artifi cial liver support system in treatment of liverfailure after acute poisoning

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World Journal of Emergency Medicine 2011年第4期2卷 283-286页

作者： Li-gang Chen bayasi guleng Jian-lin Ren Jian-min Chen Lin Wang Department of Gastroenterology Zhongshan Hospital Affi liated to Xiamen University Xiamen 361004 China

BACKGROUND： Acute poisoning （AP） may cause failure of the liver and kidney, and evendeath. This study aimed to investigate the efficacy of artificial liver support system （ALSS） on thetreatment of liver failure after acute ***： A total of 31 patients with liver failure caused by AP were admitted to emergency ICU,central ICU, and Department of Gastroenterology from 2005 to 2009 in Zhongshan Hospital Affi liatedto Xiamen University, China. Among them, 13 patients served as a treatment group, and used ALSS inaddition to detoxifi cation treatment and protective treatment of liver function, and the other 18 patientsserved as a control group receiving detoxifi cation treatment and protective treatment of liver ***： In the treatment group, 10 patients （76.9%） were cured or improved, 2 died, and1 was discharged against advice. In the 18 patients in the control group, 7 （38.9%） were cured orimproved, 3 died, and 8 were discharged against advice. There was a significant difference in therates of improvement between the two groups （P〈0.05）.CONCLUSION： ALSS is a safe and effective clinical method for the treatment of acute toxicliver failure.

关键词： Toxicity Liver failure Artifi cial liver support system

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缺氧诱导胃癌细胞SGC-7901中三叶因子3与血管内皮生长因子相互关系研究

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中华消化杂志 2012年第4期32卷 232-235页

作者：黄庆文韩佳王琳叶震世巴亚斯古楞任建林厦门大学附属中山医院消化科厦门大学消化疾病研究所厦门市消化疾病中心福建厦门361004

目的探讨在缺氧条件下胃癌细胞SGC-7901中三叶因子3（TFF3）与血管内皮生长因子（VEGF）及缺氧诱导因子（HIF—1a）的相互关系，了解TFF3在胃癌发生发展过程中的作用机制。方法使用氯化钴（CoCl2）构建胃癌细胞株SGC-7901的缺氧模型。... 详细信息

目的探讨在缺氧条件下胃癌细胞SGC-7901中三叶因子3（TFF3）与血管内皮生长因子（VEGF）及缺氧诱导因子（HIF—1a）的相互关系，了解TFF3在胃癌发生发展过程中的作用机制。方法使用氯化钴（CoCl2）构建胃癌细胞株SGC-7901的缺氧模型。运用携带靶向干扰人类TFF3的pU6-siTFF3和pU6-mock分别转染胃癌细胞株SGC-7901，以嘌呤霉素为筛选药物，建立稳定特异性抑制TFF3的胃癌细胞株。在缺氧环境和常氧环境下培养胃癌细胞株SGC-7901和靶向干扰TFF3后的胃癌细胞株SGC-7901，运用定量PCR、ELISA和Western印迹分析等方法分别测定其TFF3、HIF-1a和VEGF的蛋白和mRNA表达情况。运用免疫荧光法观察在缺氧环境和常氧环境下胃癌细胞株SGC-7901中TFF3、HIF-1a的分布及表达量。结果CoCl2缺氧处理能诱导胃癌细胞株SGC-7901中HIF-1d、TFF3和VEGFmRNA表达量上升（分别为33．4±1．8、14．8±1．1和15．1±1．2）。稳定干扰TFF3的SGC-7901细胞在缺氧诱导下能下调VEGF和HIF-1蛋白的表达。结论TFF3介导调节了缺氧条件下VEGF和HIF-1的表达，TFF3有可能是潜在的抗血管生成胃癌治疗靶点。

关键词：重组蛋白质类胃肿瘤肿瘤细胞培养的血管表皮生长因子类缺氧诱导因子 1,a亚基缺氧

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