Therapeutic effect of DA-9601 on chronic reflux gastritis induced by sodium taurocholate in rats

doi:10.3748/wjg.v11.i47.7430

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Dec 21, 2005 (publication date) through Nov 5, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Research

World J Gastroenterol. Dec 21, 2005; 11(47): 7430-7435
Published online Dec 21, 2005. doi: 10.3748/wjg.v11.i47.7430

Therapeutic effect of DA-9601 on chronic reflux gastritis induced by sodium taurocholate in rats

Tae Young Oh, Chang Yell Shin, Yong Sung Sohn, Dong Hwan Kim, Byoung Ok Ahn, Eun Bang Lee, Cho Hyun Park

Tae Young Oh, Chang Yell Shin, Yong Sung Sohn, Dong Hwan Kim, Byoung Ok Ahn, Eun Bang Lee, Dong-A Pharmaceutical Research Institute, Yongin, Korea

Cho Hyun Park, Department of General Surgery, Catholic University of Medicine, Seoul, Korea

Author contributions: All authors contributed equally to the work.

Supported by the grant from Korean Ministry of Health and Welfare, HMP-98-D-1-0007

Correspondence to: Tae Young Oh, Dong-A Pharmaceutical Research Institute, 47-5, Sanggal-ri, Kiheung-up, Yongin-shi, Kyunggi-do 449-905, Korea. solemiooh@donga.co.kr

Telephone: +82-31-280-1389 Fax: +82-31-282-8564

Received: March 31, 2005
Revised: August 2, 2005
Accepted: August 9, 2005
Published online: December 21, 2005

Abstract

AIM: To investigate the therapeutic effects of DA-9601 on sodium taurocholate (TCA)-induced chronic reflux gastritis in SD rats.

METHODS: In this study, we have investigated the therapeutic effects of DA-9601 on chronic erosive and atrophic gastritis induced by 6 mo of TCA administration (5 mmol/L in drinking water) in SD rats.

RESULTS: Four weeks of DA-9601 administration (0.065%, 0.216% in rat chow), following the withdrawal of TCA treatment, resulted in a significant decrease in total length of erosions in rats in a dose-dependent manner. Furthermore, the indicators of atrophic gastritis, such as reduced mucosal thickness and reduction in the number of parietal cells, were improved by the administration of DA-9601 in a dose-related manner. DA-9601 also attenuated inflammatory cell infiltration and the proliferation of collagenous fiber in the gastric mucosa. The improvement in the reduction of the gastric mucus was observed in the rats receiving a high dose of DA-9601 (0.216%). The therapeutic effect of DA-9601 on experimental chronic erosive gastritis was superior to that of rebamipide (1.08% in rat chow). Biochemical analyses showed increased mucosal prostaglandin E₂ and reduced glutathione levels by DA-9601 treatment.

CONCLUSION: We suggest that DA-9601 is a promising agent for the treatment of chronic erosive and atrophic gastritis with an etiological factor of bile reflux. Increased mucosal prostaglandin E₂ and reduced glutathione by DA-9601 treatment may be therapeutic mechanisms for chronic erosive and atrophic gastritis.

Keywords: DA-9601; Reflux gastritis; Erosive gastritis; Atrophic gastritis; Sodium taurocholate