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作 者:王晓娣[1]
机构地区:[1]卫生部中日友好医院消化内科,北京市100029
出 处:《世界华人消化杂志》2008年第28期3197-3199,共3页World Chinese Journal of Digestology
摘 要:炎症性肠病(inflammatory bowel disease,IBD)-是发生在胃肠道慢性非特异性炎症性疾病,其病因及发病机制尚未十分明确,可能与环境因素、遗传因素和免疫因素等有关.研究表明细胞凋亡在IBD的发病中起着重要的作用,表现为炎症肠黏膜组织内存在细胞凋亡紊乱,肠上皮细胞凋亡过度、黏膜固有层组织内淋巴细胞凋亡抵抗,以及PMN凋亡迟滞,这是造成IBD肠道炎症发生和持续的重要原因.研究发现发生细胞凋亡的主要机制在于激活了Fas/FasL信号传导途径、Bcl-2和Bax调节途径而实施的,研究细胞凋亡机制对揭示IBD的发病机制,靶向性阻断细胞凋亡通路治疗IBD发生有重要意义.Inflammatory bowel disease (IBD) is non-specific inflammatory disease in intestinal tract, and its etiology and pathogenesis are still unclear, which are probably associated with environmental factors, genetic factors and immunological factors. Studies have demonstrated that cell apoptosis plays an important role in the development of IBD, characterized by increased intestinal epithelial cell apoptosis, apoptosis resistance of intestinal lamina propria lymphocytes and apoptosis delay of polymorphonuclear neutrophils. Further studies have indicated that activation of Fas/FasL signaling transduction, Bcl-2 and Bax pathways is involved in cell apoptosis. This paper highlights the potential role of mucosal cell apoptosis in the pathogenesis and treatment of IBD.
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