The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2007
[Expression of peroxisome proliferator-activated receptor (PPAR) gamma in Helicobacter pylori-infected gastric epithelium].
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Son Seong Hyun, Kim Hyung Keun, Ji Jeong Seon, Cho Young Seok, Kim Sung Soo, Chae Hiun Suk, Choi Myung Gyu, Han Sok Won, Choi Kyu Yong, Chung In Sik, Shin Ok Ran
Аннотация
BACKGROUND/AIMS: Peroxisome proliferator-activated receptor gamma (PPAR gamma), a nuclear transcription factor, plays a critical role in the regulation of gene expression associated with inflammation and cancer. PPAR gamma is expressed in human gastric cancer as well as in colon cancer. Activation of PPAR gamma by ligand produces pro-apoptotic effect and ameliorate growing of cancer cells. Helicobacter pylori (H. pylori) is a main etiologic agent for gastric inflammation, and raises cell turnover in gastric epithelium. Longstanding infection with this organism is related with the development of non-cardiac gastric cancer. The aim of this study was to investigate the effect of H. pylori on the expression of PPAR gamma protein and mRNA in chronic gastritis.
METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPAR gamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry.
RESULTS: PPAR gamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPAR gamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPAR gamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively).
CONCLUSIONS: PPAR gamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPAR gamma in the mucosal inflammatory reaction to H. pylori infection.
METHODS: Gastric biopsy samples were taken from H. pylori infected (n=18) and non-infected (n=21) patients during endoscopic examination. PPAR gamma expressions were assessed by real time polymerase chain reaction and immunohistochemistry.
RESULTS: PPAR gamma was localized to the nuclei of the foveolar epithelial cells in both infected and non-infected mucosa. PPAR gamma protein expression was higher in H. pylori infected patients than in non-infected patients (3.8+/-0.4 vs. 2.6+/-1.0, H. pylori infected and non-infected, respectively; p<0.05). However, PPAR gamma mRNA levels were not significantly different between the two groups (24+/-18 vs. 29+/-25, H. pylori infected and noninfected, respectively).
CONCLUSIONS: PPAR gamma expression is increased in the gastric mucosa of H. pylori infected chronic gastritis, which suggests a certain role of PPAR gamma in the mucosal inflammatory reaction to H. pylori infection.