15-脱氧-Δ12,14-前列腺素J2抑制核因子-κB介导的幽门螺杆菌感染的胃上皮细胞凋亡。
15-Deoxy-delta 12, 14,-prostaglandin J2 suppresses nuclear factor-kappaB-mediated apoptosis of Helicobacter pylori-infected gastric epithelial cells.
作者信息
Cha Boram, Kim Kyung Hwan, Kim Hyeyoung
机构信息
Department of Pharmacology and Institute of Gastroenterology, Brain Korea 21 Project, Yonsei University College of Human Ecology, Seoul, Korea.
出版信息
Ann N Y Acad Sci. 2009 Aug;1171:457-63. doi: 10.1111/j.1749-6632.2009.04706.x.
Helicobacter pylori deregulates the genes that control homeostasis between apoptosis and cell proliferation of gastric epithelial cells. Nuclear factor-kappaB (NF-kappaB) has an important role in H. pylori-induced apoptosis in gastric epithelial cells. The peroxisome proliferator-activated receptor-gamma ligand 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) regulates growth and the signaling cascade in H. pylori-infected gastric epithelial cells. In the present study, we determined whether 15d-PGJ(2) inhibits apoptosis by regulating apoptotic gene expression and NF-kappaB activation in gastric epithelial cells infected with CagA+, VacA+H. pylori in a Korean isolate (HP99). 15d-PGJ(2) was found to inhibit H. pylori-induced DNA fragmentation and cell death. 15d-PGJ(2) induced downregulation of proapoptotic Bax and upregulation of antiapoptotic Bcl-2 as well as suppression of NF-kappaB activation caused by H. pylori in gastric epithelial cells. The results suggest that 15d-PGJ(2) inhibits apoptotic cell death by inhibiting NF-kappaB activation and apoptotic gene expression in gastric epithelial cells.
幽门螺杆菌会破坏控制胃上皮细胞凋亡与细胞增殖之间稳态的基因。核因子-κB（NF-κB）在幽门螺杆菌诱导的胃上皮细胞凋亡中起重要作用。过氧化物酶体增殖物激活受体-γ配体15-脱氧-Δ（12,14）-前列腺素J2（15d-PGJ2）调节幽门螺杆菌感染的胃上皮细胞的生长和信号级联反应。在本研究中，我们确定15d-PGJ2是否通过调节感染CagA+、VacA+的韩国分离株（HP99）幽门螺杆菌的胃上皮细胞中的凋亡基因表达和NF-κB激活来抑制凋亡。发现15d-PGJ2可抑制幽门螺杆菌诱导的DNA片段化和细胞死亡。15d-PGJ2可诱导胃上皮细胞中促凋亡蛋白Bax的下调和抗凋亡蛋白Bcl-2的上调，以及抑制幽门螺杆菌引起的NF-κB激活。结果表明，15d-PGJ2通过抑制胃上皮细胞中的NF-κB激活和凋亡基因表达来抑制凋亡性细胞死亡。
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