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本文引用的文献

1
Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites.幽门螺杆菌胃炎不同胃部位的胃上皮细胞增殖及cagA状态
Scand J Gastroenterol. 2007 May;42(5):545-54. doi: 10.1080/00365520601014034.
2
The role of Helicobacter pylori CagA in gastric carcinogenesis.幽门螺杆菌细胞毒素相关基因A(CagA)在胃癌发生中的作用。
Int J Hematol. 2006 Nov;84(4):301-8. doi: 10.1532/IJH97.06166.
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Helicobacter pylori CagA: a new paradigm for bacterial carcinogenesis.幽门螺杆菌CagA:细菌致癌作用的新范例。
Cancer Sci. 2005 Dec;96(12):835-43. doi: 10.1111/j.1349-7006.2005.00130.x.
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Local and systemic immune and inflammatory responses to Helicobacter pylori strains.针对幽门螺杆菌菌株的局部和全身免疫及炎症反应。
Clin Diagn Lab Immunol. 2005 Dec;12(12):1393-400. doi: 10.1128/CDLI.12.12.1393-1400.2005.
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Differential expression of connexin 43 in gastrointestinal stromal tumours of gastric and small intestinal origin.胃和小肠来源的胃肠道间质瘤中连接蛋白43的差异表达
J Pathol. 2005 Aug;206(4):377-82. doi: 10.1002/path.1799.
6
Development of gastric adenocarcinoma in Mongolian gerbils after long-term infection with Helicobacter pylori.幽门螺杆菌长期感染后蒙古沙鼠胃腺癌的发生
J Gastroenterol Hepatol. 2004 Oct;19(10):1192-8. doi: 10.1111/j.1440-1746.2004.03469.x.
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Effects of Helicobacter pylori on endothelial cell proliferation and chemotaxis.
Digestion. 2004;69(4):201-10. doi: 10.1159/000079149. Epub 2004 Jun 16.
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Gastric cancer epidemiology and risk factors.胃癌流行病学与风险因素
J Clin Epidemiol. 2003 Jan;56(1):1-9. doi: 10.1016/s0895-4356(02)00534-6.
9
Effect of Helicobacter pylori infection on gastric epithelial cell proliferation.幽门螺杆菌感染对胃上皮细胞增殖的影响。
World J Gastroenterol. 2000 Jun;6(3):442-444. doi: 10.3748/wjg.v6.i3.442.
10
Inhibition of connexin43 gap junctional intercellular communication by TPA requires ERK activation.佛波酯对连接蛋白43间隙连接细胞间通讯的抑制作用需要细胞外信号调节激酶的激活。
J Cell Biochem. 2001;83(1):163-9. doi: 10.1002/jcb.1227.

幽门螺杆菌感染对体外胃上皮细胞间隙连接细胞间通讯及增殖的影响。

Effects of H pylori infection on gap-junctional intercellular communication and proliferation of gastric epithelial cells in vitro.

作者信息

Tao Ran, Hu Miao-Feng, Lou Jin-Tu, Lei Yong-Liang

机构信息

Central Laboratory, Children's Hospital, School of Medicine, Zhejiang University, 57 Zhugan Lane, Hangzhou 310003, Zhejiang Province, China.

出版信息

World J Gastroenterol. 2007 Nov 7;13(41):5497-500. doi: 10.3748/wjg.v13.i41.5497.

DOI:10.3748/wjg.v13.i41.5497
PMID:17907295
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4171286/
Abstract

AIM

To explore the effects of H pylori infection on gap-junctional intercellular communication (GJIC) and proliferation of gastric epithelial cells in vitro.

METHODS

A human gastric epithelial cell line (SGC-7901) cultured on coverslips was exposed overnight to intact H pylori (CagA(+) or CagA(-) strains) and sonicated extracts, respectively. GJIC between the cells was detected by fluorescence redistribution after photobleaching (FRAP) technique. Proliferation of SGC cells was determined by methylthiazolyl tetrazolium (MTT) assay.

RESULTS

When compared with control in which cells were cultured with simple medium alone, both CagA(+) and CagA(-) H pylori isolates could inhibit GJIC (CagA(+): F = 57.98, P < 0.01; CagA(-): F = 29.59, P < 0.01) and proliferation (CagA(+): F = 42.65, P < 0.01; CagA(-): F = 58.14, P < 0.01) of SGC-7901 cells. Compared with CagA(-) strains, CagA(+) H pylori more significantly down-regulated GJIC of gastric cells (intact H pylori: t = 13.86, P < 0.01; sonicated extracts: t = 11.87, P < 0.01) and inhibited proliferation gastric cells to a lesser extent in vitro (intact H pylori: t = 3.06, P < 0.05; sonicated extracts: t = 3.94, P < 0.01).

CONCLUSION

Compared with CagA(-) H pylori strains, CagA(+) strains down-regulate GJIC of gastric epithelial cells more significantly and inhibit proliferation of gastric cells to a lesser extent in vitro. H pylori, especially CagA(+) strains, may play an important role in gastric carcinogenesis.

摘要

目的

探讨幽门螺杆菌感染对体外胃上皮细胞间隙连接细胞通讯(GJIC)及增殖的影响。

方法

将培养在盖玻片上的人胃上皮细胞系(SGC-7901)分别用完整的幽门螺杆菌(细胞毒素相关基因A阳性或阴性菌株)和超声破碎提取物处理过夜。采用光漂白后荧光再分布(FRAP)技术检测细胞间的GJIC。通过甲基噻唑基四氮唑(MTT)法测定SGC细胞的增殖。

结果

与仅用单纯培养基培养细胞的对照组相比,细胞毒素相关基因A阳性和阴性幽门螺杆菌分离株均可抑制SGC-7901细胞的GJIC(细胞毒素相关基因A阳性:F = 57.98,P < 0.01;细胞毒素相关基因A阴性:F = 29.59,P < 0.01)及增殖(细胞毒素相关基因A阳性:F = 42.65,P < 0.01;细胞毒素相关基因A阴性:F = 58.14,P < 0.01)。与细胞毒素相关基因A阴性菌株相比,细胞毒素相关基因A阳性幽门螺杆菌更显著地下调胃细胞的GJIC(完整幽门螺杆菌:t = 13.86,P < 0.01;超声破碎提取物:t = 11.87,P < 0.01),且在体外对胃细胞增殖的抑制作用较小(完整幽门螺杆菌:t = 3.06,P < 0.05;超声破碎提取物:t = 3.94,P < 0.01)。

结论

与细胞毒素相关基因A阴性幽门螺杆菌菌株相比,细胞毒素相关基因A阳性菌株更显著地下调胃上皮细胞的GJIC,且在体外对胃细胞增殖的抑制作用较小。幽门螺杆菌,尤其是细胞毒素相关基因A阳性菌株,可能在胃癌发生中起重要作用。