细胞凋亡与溃疡性结肠炎关系的研究进展

溃疡性结肠炎(UC)的病因和发病机制目前尚不明确。近年来研究发现,结肠相关黏膜细胞凋亡失控在UC的发病中起着重要作用,其中肠黏膜上皮细胞凋亡加速、固有层T淋巴细胞和中性粒细胞等炎性细胞凋亡延迟可能与UC的发生、发展密切相关。不同细胞发生凋亡分别受CD95、Apo-2.7、Bcl-2、核因子κB等基因的调控,在UC发病机制中CD95、Apo-2.7主要加速上皮细胞凋亡,Bcl-2、核因子κB主要抑制淋巴细胞和中性粒细胞等炎性细胞凋亡,引起肠黏膜上皮损伤和炎性细胞浸润,促使UC发病。

Cell Apoptosis and Ulcerative Colonitis

The etiology and pathogenesis of ulcerative colitis(UC)remain unclear now.The recent studies have shown that the abnormal change in intestinal mucosal apoptosis plays a significant role in the pathogenesis of UC.The acceleration of apoptosis in colonic epithelial cells and suppression of apoptosis in intestinal lamina propria T-lymphocytes,neutrophils,and other inflammatory cells may contribute to the occurrence and progression of UC.Apoptosis is controlled by some genes,such as CD95,Apo-2.7,Bcl-2 and nuclear factor B in UC.CD95 and Apo-2.7 mainly accelerate the epithelial cell apoptosis,whereas Bcl-2 and nuclear factor B mainly inhibit the apoptosis in lymphocytes,neutrophils and other inflammatory cells,impairing intestinal epithelia,inducing inflammatory cell infiltration,and promoting the occurrence of UC.