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幽门螺旋杆菌对慢性胃炎患者粘膜内D细胞及生长抑素mRNA表达的影响 被引量:2

THE EFFECT OF HELICOBACTER PYLORI INFECTION ON THE EXPRESSION OF D CELL AND SOMATOSTATIN mRNA IN THE PATIENTS WITH CHRONIC GASTRITIS
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摘要 目的 了解幽门螺旋杆菌 (Hp)感染与慢性胃炎患者胃窦粘膜内D细胞及生长抑素mRNA+ 细胞 (DmRNA+ 细胞 )减少的关系。 方法 免疫细胞化学和原位杂交技术。 结果 正常组D细胞与Hp- 胃炎组无差别(P >0 0 5 ) ,但Hp+ 胃炎组D细胞显著减少 ,与Hp- 胃炎组相比有显著性差异 (P <0 0 1)。DmRNA+ 细胞 ,Hp+ 胃炎组也低于其他 2组且有显著性差异 (P <0 0 1)。 结论 Hp+ 胃炎组内D细胞及DmRNA+ 细胞减少与Hp感染有密切关系。它能减少D细胞分泌的生长抑素对G细胞分泌的影响 ,但是生长抑素基因的转录和蛋白的合成依然运行。 Objective To investigate the relationship between D cells and somatostatin mRNA + cells decreased in the antral mucosa of patients with chronic gastritis and helicobacter pylori infection. Methods Immunocytochemistry and in situ hybridization. Results The results indicated that the number of D cells was not obvious different between the control and HP+- groups(P>0.05), but in the HP + group, the D cells markedly reduced as compared with HP - group and showed a significantly difference(P<0.01). Somatostatin mRNA + cells in the HP + gastritis group was also lower than that of the other two groups, and had a significant difference (P<0.01).Conclusion The D cells and somatostatin mRNA + cells decreased in the HP + group closely related to the Hp infection, which can be able to reduce the inhibition of G cell's secretion by D cell producing somatostatin, but the transcription of somatostatin gene and protein synthesis were runing well.
出处 《解剖学报》 CAS CSCD 北大核心 2004年第1期88-91,共4页 Acta Anatomica Sinica
基金 福建省卫生厅科研基金资助课题 ( 960 5 7)
关键词 幽门螺旋杆菌 慢性胃炎 粘膜内D细胞 生长抑素 MRNA 表达 Chronic gastritis D cells Somatostatin mRNA + cells Immunocytochemistry in situ hybridization Helicobacter pylori
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  • 1[1]Larsson LI, Hougaard DM. Evidence for paracrine somatostatinergic regulation of gastrin gene expression by double staining cytochemistry and quantitation [J]. J Histochem Cytochem,1994,42(1):37-40.
  • 2[2]Calam J. Helicobacter pylori and somatostatin cells [J]. Eur J Gastroenterol hepatol,1998,10(4):281-283.
  • 3[3]Huang SM, Lin HH, Wen TY, et al. Extreme hypergastrinemia by atrophic gastritis and helicobacter pylori infection-a case report [J]. Hepatogastroenterology,2001,48(40):1215-1216.
  • 4[4]Larsson LI, Hougaard DM. Non-radioactive in situ mRNA hybridization using synthetic oligonucleotides:principles combination with immunocytochemistry and quantitation [J]. Neurosci Protocols,1993,20(6):1-18.
  • 5[8]Zavros Y, Paterson A, Lambert J, et al. Expression of progastrin-derived peptides and somatostatin in fundus and antrum of nonulcer dyspepsia subjects with and without helicobacter pylori infection [J]. Dig Dis Sci,2000,45(10):2058-2064.
  • 6[9]Mihaljevic S, Kaicic M, Karner I, et al. The influence of helicobacter pylori infection on gastrin and somatostatin values present in serum [J]. Hepatogastroenterology,2000,47(35):1482-1484.
  • 7[10]Lchmann FS, Beglinger C. Significance of cytokines for pathophysiology and clinical aspects of helicobacter pylori [J]. Schweiz Med Wochenscher,20001,130(7):240-248.
  • 8[11]Lamberts R, Stumps D, Plümpe L, et al. Somatostatin cells in rat antral mucosa:Qualitative and quantitative ultrastructural analyses in different states of gastric acid secretion [J]. Histochemistry,1991,95(2):373-382.

同被引文献30

  • 1唐咏梅,刘海芳.幽门螺旋杆菌与慢性活动性胃炎的临床和病理[J].华南国防医学杂志,2002,16(4):24-25. 被引量:4
  • 2蒋桂芳,李国维,李美玲.泰州地区幽门螺旋杆菌的发病情况调查[J].南京医学院学报,1994,14(1):121-121. 被引量:2
  • 3Saitoh T,Iochizuki T, Suda T, et al. Elevation of TFF1 gene expression during of healing of gastric ulcer at no-ulcerated sited in stomach: semiquantification using the single tube method of polymerase chain reaction. J Gastroenterol Hepatol, 2000,15(6):604-609.
  • 4Coyle WJ, Sedlack RE, Nemec R, et al. Eradication of helicobacter pylori normalizes elevated mucosal level of EGF and its receptor. Am J Gastoenterol, 1999,94(10):2885-2889.
  • 5Schiemann U, Konturek JW, Osterhoff I, et al. Decreased expression of EGF-R and mRNA of its ligands in helicobacter pylori-infected gastric mucosa. Scan J Gastroenterol, 2001,36(1):23-31.
  • 6Pai R, Sasaki E,Tarnawski AS. Helicobacter pylori: Vacuolating cytotoxin(VacA) alters cytoskeleton associated proteins and interfers with re-epitheliallization of wounded gastric epitheilal monolayers. Cell Biol Int,2000,24(5):291-330.
  • 7Taupin D, Pedersen J, Familari I, et al.Augmented interstinal trefoil factor(TFF3) and lose of TFF1 expression precedes metaplastic differentiation of gastric epithelium. Lab Invest, 2001,81(3):397-408.
  • 8Beckler AD, Roche JK, Harper JC, et al. Decrease abundance of trefoil factor1 transcript in majority of gastric carcinoma. Cancer,2003,98(10):2184-2191.
  • 9Beales IL. Effect of platelet-activating factor on gastrin release from cultured rabbit G-cells. Dig Dis Sci, 2001,46(2):301-306.
  • 10Mihaljevic S, Kaicik M, Karner I, et al. The influence of helicobacter pylori infection on gastrin and somatostatin values present in serum. Hepatogastroenterology,2000,97(35):1482-1484.

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