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上调的环氧化酶-2抑制幽门螺杆菌感染的人胃上皮细胞凋亡。

Upregulated cyclooxygenase-2 inhibits apoptosis of human gastric epithelial cells infected with Helicobacter pylori.

作者信息

Kim J M, Kim J S, Jung H C, Song I S, Kim C Y

机构信息

Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.

出版信息

Dig Dis Sci. 2000 Dec;45(12):2436-43. doi: 10.1023/a:1005611613542.

Abstract

Helicobacter pylori induces apoptosis and alters the proliferation of gastric mucosal epithelial cells. Cyclooxygenase-2 (COX-2), the inducible form of prostaglandin (PG) synthesis, is known to cause alteration in epithelial cell growth. The goal of this study was to determine whether COX-2 gene expression by H. pylori infection could influence gastric epithelial cell apoptosis. Expression of COX-2 mRNA and proteins was up-regulated in Hs746T gastric epithelial cell lines infected with H. pylori, when assessed by quantitative RT-PCR and western blot. Inhibition of COX-2 expression using NS-398, a specific COX-2 inhibitor, showed a significant increase of gastric epithelial cell apoptosis and caspase-3 activation in Hs746T cells infected with H. pylori. Moreover, the effect of NS-398 on H. pylori-induced apoptosis was reversed by the addition of PGE2. These results suggest that up-regulated COX-2 expression by H. pylori infection can inhibit apoptosis of gastric epithelial cells.

摘要

幽门螺杆菌可诱导胃黏膜上皮细胞凋亡并改变其增殖。环氧化酶-2(COX-2)是前列腺素(PG)合成的诱导形式,已知其会引起上皮细胞生长的改变。本研究的目的是确定幽门螺杆菌感染导致的COX-2基因表达是否会影响胃上皮细胞凋亡。通过定量逆转录聚合酶链反应(RT-PCR)和蛋白质印迹法评估发现,感染幽门螺杆菌的Hs746T胃上皮细胞系中COX-2信使核糖核酸(mRNA)和蛋白质的表达上调。使用特异性COX-2抑制剂NS-398抑制COX-2表达后,感染幽门螺杆菌的Hs746T细胞中胃上皮细胞凋亡和半胱天冬酶-3激活显著增加。此外,添加前列腺素E2(PGE2)可逆转NS-398对幽门螺杆菌诱导凋亡的影响。这些结果表明,幽门螺杆菌感染导致的COX-2表达上调可抑制胃上皮细胞凋亡。

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