期刊文献+

非可控性炎症对Hp相关胃病恶性演变与中医证候研究的启示 被引量:4

Investigative hypothesis regarding the malignant evolution of kelicobacter pylori-related gastric disease and Chinese medicine syndromes via non-resolving inflammation
原文传递
导出
摘要 非可控性炎症(NRI)是宿主、机体微环境与病原微生物相互作用的复杂病理过程,作为炎症的中心环节,NF-κB信号通路和microRNA分子异常所致的炎症因子、趋化因子异常表达,以及炎性细胞功能的失调,可能是幽门螺杆菌相关胃病(HPGD)NRI发生的分子基础;文章初步提出"邪毒致变"的观点,并据此探讨HPGD恶性演变过程中,炎性微环境改变与不同中医证候特征关联的可能性。 Non-resolving inflammation(NRI) is a complex pathological process of the interaction between the microenvironment of the host,body's microenvironment and pathogenic microorganisms.The molecular basis for the occurrence of NRI in Helicobacter pylori-related gastric disease(HPGD) is likely due to the functional disorder of inflammatory cytokines,chemokines and cells caused by an abnormal micro RNA molecule and an abnormality within the NF-κB signaling pathway which is a central component of inflammation.This article initially proposed the perspective of 'pathogenic-toxin caused malignant transformation' and discussed a possible relationship between the change in the inflammatory microenvironment that occurs during the process of the malignant evolution of HPGD and the features of different TCM syndromes.
出处 《中华中医药杂志》 CAS CSCD 北大核心 2017年第4期1561-1563,共3页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 国家自然科学基金项目(No.81373563) 广东省自然科学基金项目(No.S2012010010355) 中央财政支持地方高校发展专项资金项目[No.财教(2013)338号] 广州中医药大学"创新研究团队"项目(No.2016KYTD07) 广州中医药大学"高水平大学建设"项目[No.广中医研(2016)64号]~~
关键词 非可控性炎症 Hp相关胃病 恶性演变 中医证候 Non-resolving inflammation Helicobacter pylori-related gastric disease Malignant evolution Syndromes of Chinese medicine
  • 相关文献

参考文献2

二级参考文献21

  • 1舒惠荃,王宝山,刘志勇,曹颖颖.正邪交争与炎性反应[J].现代中西医结合杂志,2006,15(16):2157-2158. 被引量:6
  • 2中国慢性胃炎共识意见[J].胃肠病学,2006,11(11):674-684. 被引量:835
  • 3Yanai A, Maeda S, Shibata W,et al. Activation of kappaB kinase and NF-KappaB is essential for Helicobacter pyloriinduced chronic gastritis in Mongolian gerbils [ J ]. Infect Immun, 2008,76(2) :781-787.
  • 4Kirn SY, Lee YC, Kim HK, et al. Helicobacter pylori CagA transfeetion of gastric epithelial cells induees interleukin - 8 [ J]. Cell Microbiol,2006,8 ( 1 ) :97- 106.
  • 5Yeo M,Park HK, Kim DK,et al. Restoration of heat shock protein 70 suppresses gastric mucosal inducible nitric oxide synthase expression induced by Helicobacter pylori [ J ]. Proteomics,2004,4( 11 ) :3335- 3342.
  • 6Zheng Z, Kim JY, Ma H, et al. Anti - inflammatory effects of the 70 kDa heat shock protein in experimental stroke [J]. J Cereb Blood Flow Metab, 2008,28(1):53-63.
  • 7Schell MT, Spitzer AL, Johnson JA, et al. Heat shock inhibits NF-κB activation in a dose-and time-dependent manner[ J]. J Surg Res, 2005,129 (1) :90- 93.
  • 8Pierzchalski P, Krawiec A, Ptak - Belowska A, et al. The mechanism of heat-shock protein 70 gene expression abolition in gastric epithelium caused by Helicobacter pylori infection [ J ]. Helicobacter, 2006,11 ( 2 ) : 96- 104.
  • 9Konturek SJ, Konturek PC, konturek JW, et al. Helicobacter pylori and its involvement in gastritis and peptic ulcer formation[ J]. J Physiol Pharmacol, 2006,57 ( 3 ) :29- 50.
  • 10杨桂彬,魏红,胡伏莲,牟方宏,崔梅花.安速快速检测试剂盒诊断幽门螺杆菌的现症感染[J].世界华人消化杂志,2007,15(23):2545-2548. 被引量:13

共引文献34

同被引文献54

引证文献4

二级引证文献22

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部