Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage

K. W. Choi; Y. C. Lee; I. S. Chung; J. J. Lee; M. H. Chung; N. Y. Kim; S. W. Kim; J. G. Kim; I. H. Roe; S. W. Lee; H. Y. Jung; M. G. Choi; K. B. Hahm; W. S. Hong; J. H. Kim

doi:10.1023/A:1013753602149

Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage

K. W. Choi, Y. C. Lee, I. S. Chung, J. J. Lee, M. H. Chung, N. Y. Kim, S. W. Kim, J. G. Kim, I. H. Roe, S. W. Lee, H. Y. Jung, M. G. Choi, K. B. Hahm, W. S. Hong, J. H. Kim

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

Production of cytokines along with increased activity of nitric oxide synthase has been implicated as one of the contributing mechanisms of Helicobacter pylori-mediated gastroduodenal diseases. We aimed to evaluate the effect of rebamipide in treating Helicobacter pylori-associated duodenal ulcers in terms of cytokine production and nitrosative damage of the gastric mucosa. In patients with duodenal ulcers, rebamipide or placebo were given randomly after eradication. Mucosal cytokine production was measured by enzyme linked immunoassay, and nitrotyrosine immunoexpression was measured by immunohistochemistry. The inflammatory activity and degree of neutrophil infiltration were graded accordingly. The mucosal production of RANTES, interleukin-8, and TNF-α showed a significant decrease after eradication in patients with rebamipide after-treatment. The nitrotyrosine immunoreactivity of gastric epithelium was significantly decreased in the rebamipide group. Rebamipide treatment after eradication resulted in a significant reduction in chemokine production along with nitrotyrosine immunoexpression in Helicobacter pylori-associated duodenal ulcers.

Original language	English
Pages (from-to)	283-291
Number of pages	9
Journal	Digestive diseases and sciences
Volume	47
Issue number	2
DOIs	https://doi.org/10.1023/A:1013753602149
Publication status	Published - 2002

Bibliographical note

Funding Information:
This study was supported in part by a grant from Korea Otsuka Pharmaceuticals.

All Science Journal Classification (ASJC) codes

Physiology
Gastroenterology

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10.1023/A:1013753602149

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Choi, K. W., Lee, Y. C., Chung, I. S., Lee, J. J., Chung, M. H., Kim, N. Y., Kim, S. W., Kim, J. G., Roe, I. H., Lee, S. W., Jung, H. Y., Choi, M. G., Hahm, K. B., Hong, W. S., & Kim, J. H. (2002). Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage. Digestive diseases and sciences, 47(2), 283-291. https://doi.org/10.1023/A:1013753602149

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title = "Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage",

abstract = "Production of cytokines along with increased activity of nitric oxide synthase has been implicated as one of the contributing mechanisms of Helicobacter pylori-mediated gastroduodenal diseases. We aimed to evaluate the effect of rebamipide in treating Helicobacter pylori-associated duodenal ulcers in terms of cytokine production and nitrosative damage of the gastric mucosa. In patients with duodenal ulcers, rebamipide or placebo were given randomly after eradication. Mucosal cytokine production was measured by enzyme linked immunoassay, and nitrotyrosine immunoexpression was measured by immunohistochemistry. The inflammatory activity and degree of neutrophil infiltration were graded accordingly. The mucosal production of RANTES, interleukin-8, and TNF-α showed a significant decrease after eradication in patients with rebamipide after-treatment. The nitrotyrosine immunoreactivity of gastric epithelium was significantly decreased in the rebamipide group. Rebamipide treatment after eradication resulted in a significant reduction in chemokine production along with nitrotyrosine immunoexpression in Helicobacter pylori-associated duodenal ulcers.",

author = "Choi, {K. W.} and Lee, {Y. C.} and Chung, {I. S.} and Lee, {J. J.} and Chung, {M. H.} and Kim, {N. Y.} and Kim, {S. W.} and Kim, {J. G.} and Roe, {I. H.} and Lee, {S. W.} and Jung, {H. Y.} and Choi, {M. G.} and Hahm, {K. B.} and Hong, {W. S.} and Kim, {J. H.}",

note = "Funding Information: This study was supported in part by a grant from Korea Otsuka Pharmaceuticals.",

year = "2002",

doi = "10.1023/A:1013753602149",

language = "English",

volume = "47",

pages = "283--291",

journal = "American Journal of Digestive Diseases",

issn = "0002-9211",

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Choi, KW, Lee, YC, Chung, IS, Lee, JJ, Chung, MH, Kim, NY, Kim, SW, Kim, JG, Roe, IH, Lee, SW, Jung, HY, Choi, MG, Hahm, KB, Hong, WS & Kim, JH 2002, 'Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage', Digestive diseases and sciences, vol. 47, no. 2, pp. 283-291. https://doi.org/10.1023/A:1013753602149

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T1 - Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer

T2 - Attenuation of chemokine expression and nitrosative damage

AU - Choi, K. W.

AU - Lee, Y. C.

AU - Chung, I. S.

AU - Lee, J. J.

AU - Chung, M. H.

AU - Kim, N. Y.

AU - Kim, S. W.

AU - Kim, J. G.

AU - Roe, I. H.

AU - Lee, S. W.

AU - Jung, H. Y.

AU - Choi, M. G.

AU - Hahm, K. B.

AU - Hong, W. S.

AU - Kim, J. H.

N1 - Funding Information: This study was supported in part by a grant from Korea Otsuka Pharmaceuticals.

PY - 2002

Y1 - 2002

N2 - Production of cytokines along with increased activity of nitric oxide synthase has been implicated as one of the contributing mechanisms of Helicobacter pylori-mediated gastroduodenal diseases. We aimed to evaluate the effect of rebamipide in treating Helicobacter pylori-associated duodenal ulcers in terms of cytokine production and nitrosative damage of the gastric mucosa. In patients with duodenal ulcers, rebamipide or placebo were given randomly after eradication. Mucosal cytokine production was measured by enzyme linked immunoassay, and nitrotyrosine immunoexpression was measured by immunohistochemistry. The inflammatory activity and degree of neutrophil infiltration were graded accordingly. The mucosal production of RANTES, interleukin-8, and TNF-α showed a significant decrease after eradication in patients with rebamipide after-treatment. The nitrotyrosine immunoreactivity of gastric epithelium was significantly decreased in the rebamipide group. Rebamipide treatment after eradication resulted in a significant reduction in chemokine production along with nitrotyrosine immunoexpression in Helicobacter pylori-associated duodenal ulcers.

AB - Production of cytokines along with increased activity of nitric oxide synthase has been implicated as one of the contributing mechanisms of Helicobacter pylori-mediated gastroduodenal diseases. We aimed to evaluate the effect of rebamipide in treating Helicobacter pylori-associated duodenal ulcers in terms of cytokine production and nitrosative damage of the gastric mucosa. In patients with duodenal ulcers, rebamipide or placebo were given randomly after eradication. Mucosal cytokine production was measured by enzyme linked immunoassay, and nitrotyrosine immunoexpression was measured by immunohistochemistry. The inflammatory activity and degree of neutrophil infiltration were graded accordingly. The mucosal production of RANTES, interleukin-8, and TNF-α showed a significant decrease after eradication in patients with rebamipide after-treatment. The nitrotyrosine immunoreactivity of gastric epithelium was significantly decreased in the rebamipide group. Rebamipide treatment after eradication resulted in a significant reduction in chemokine production along with nitrotyrosine immunoexpression in Helicobacter pylori-associated duodenal ulcers.

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AN - SCOPUS:0036161770

SN - 0002-9211

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JO - American Journal of Digestive Diseases

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ER -

Effect of rebamipide in treatment of Helicobacter pylori-associated duodenal ulcer: Attenuation of chemokine expression and nitrosative damage

Abstract

Bibliographical note

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