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15‐Deoxy‐Δ, 12,14 ‐prostaglandin J 2 Suppresses Nuclear Factor‐κB‐Mediated Apoptosis of Helicobacter pylori ‐Infected Gastric Epithelial Cells
Author(s) -
Cha Boram,
Kim Kyung Hwan,
Kim Hyeyoung
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.04706.x
Subject(s) - helicobacter pylori , apoptosis , prostaglandin , chemistry , microbiology and biotechnology , physics , cancer research , biology , medicine , biochemistry
Helicobacter pylori deregulates the genes that control homeostasis between apoptosis and cell proliferation of gastric epithelial cells. Nuclear factor‐κB (NF‐κB) has an important role in H. pylori ‐induced apoptosis in gastric epithelial cells. The peroxisome proliferator‐activated receptor‐γ ligand 15‐deoxy‐Δ 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‐κB 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‐κB activation caused by H. pylori in gastric epithelial cells. The results suggest that 15d‐PGJ 2 inhibits apoptotic cell death by inhibiting NF‐κB activation and apoptotic gene expression in gastric epithelial cells.