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대한Helicobacter 연구학회지 2003;3(2):96-101.
Published online November 30, 2003.
The Expression of Nitric Oxide Synthase Isotypes in Gastric Mucosa of the Patients with Chronic Gastritis before and after Helicobacter pylori Eradication
Helicobacter pylori 제균이 위점막 Nitric Oxide Synthase 아형의 발현에 미치는 영향
홍수진·권계원*·김환열·정인섭·고봉민·장재영·유창범·김진오·조주영·이준성·이문성·심찬섭·김부성
순천향대학교 의과대학 내과학교실, 소화기연구소, *병리학교실
Abstract
Backgrounds/Aims: H. pylori infection leads to the expression of iNOS and sustained production of nitric oxide in gastric mucosa. nNOS and eNOS immunoreactivity in rat in the midportion of the glands, which was identified as parietal cells in hematoxylin and eosin-stained step sections recently. We investigated patterns of NOS isotypes(iNOS, nNOS, eNOS) expression in the non-ulcerated areas to evaluate their relation to the severity of gastritis, presence of atrophy and intestinal metaplasia, or the status of H. pylori. Methods: Endoscopic mucosal biopsy specimens were taken from the patients diagnosed with chronic gastritis. The expressions of NOS isotypes were confirmed by immunohistochemistry. The immunoreactivity for NOS isotypes was compared with that after eradication therapy for H. pylori. Results: Forty-two patients were studied of whom 32 had H. pylori-associated chronic gastritis(Hp-gastritis). The iNOS expression score in the patients with H. pylori infection was higher than those without H. pylori infection(3.9 vs. 1.1, p<0.001). A decrease in immunostaining for iNOS was observed after H. pylori eradication(3.9 vs 2.1, p<0.001). There was no significant relationship between nNOS or eNOS expression and H. pylori status. There was no significant correlation between any of the NOS isotypes and the severity of gastritis, whereas the gastric epithelia with intestinal metaplasia tended to have higher activity of iNOS than adjacent areas without intestinal metaplasia before and after H. pylori eradication. Conclusions: H. pylori eradication caused significant decrease in iNOS expression. Intestinal metaplasia as a possibly precancerous lesion is a source of continuous iNOS induction even after H. pylori eradication. H. pylori infection does not affect the level of nNOS or eNOS expression in the patients with chronic gastritis. (Korean J Helicobacter Res Prac 2003;3:96-101)
Key Words: Helicobacter pylori, Nitric oxide synthase, Chronic gastritis,


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