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幽门螺杆菌诱导的胃黏膜上皮细胞凋亡机制的研究进展 被引量:2

Advances in Resarch on Mechanisms of Gastric Epithelial Cells Apoptosis Induced by Helicobacter Pylori
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摘要 胃上皮细胞不断发生凋亡和增殖,两者协同作用,从而维持了胃上皮的完整性。目前,已发现多种凋亡诱发因素。在幽门螺杆菌(HP)诱发的胃炎中,虽然上皮细胞凋亡和增殖均增加,但由于细胞凋亡占优势,破坏了胃上皮细胞的完整性而导致相关疾病的发生,其凋亡的发生机制复杂并且相互影响。由幽门螺杆菌引起的胃黏膜上皮细胞凋亡包括内源性和外源性通路,存在于这两种通路中的具有代表性的因子包括Toll样受体4、Bcl-2家族、肿瘤坏死因子相关的凋亡诱导配体/受体和Fas/FasL等。 Apoptosis and proliferation happen in gastric epithelial cells continually,which act in synergy to maintain the integrity of gastric epithelium.So far,many different factors inducing cells apoptosis have been discovered.Both the occurrence of cell apoptosis and prolifiration increased in gastritis induced by Helicobacter pylori(HP),but the former is in a dominant position,which disdrupts the integrity of gastric epithelium,leading to the occurrence of the related diseases.The mechanisms of the apoptosis are complicated and interplayed with each other.The intrinsic and extrinsic pathways are involved in the apoptotic process of the gastric epithelial cells induced by HP,during which the typical factors are involved,such as Toll-like receptor 4,Bcl-2 family,tumor necrosis factor-related apoptosis-inducing ligand/receptors,Fas/FasL,etc..
出处 《医学综述》 2011年第20期3051-3053,共3页 Medical Recapitulate
基金 江苏省教育厅自然科学基金(09KJD310009) 徐州市社会发展科技计划项目(xzzd1051) 徐州医学院院长基金(09KJZ17 09KJZ33)
关键词 幽门螺杆菌 TOLL样受体4 BCL-2家族 肿瘤坏死因子相关的凋亡诱导配体/受体Fas/FasL Helicobacter pylori Toll-like receptor 4 Bcl-2 family Tumor necrosis factorrelated apoptosis-inducing ligand/receptors Fas/FasL
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