Basic Research
Copyright ©2005 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jan 21, 2005; 11(3): 357-361
Published online Jan 21, 2005. doi: 10.3748/wjg.v11.i3.357
Effect of lipopolysaccharide on diarrhea and gastrointestinal transit in mice: Roles of nitric oxide and prostaglandin E2
Yu-Chih Liang, Hung-Jung Liu, Sheng-Hsuan Chen, Chun-Chin Chen, Liang-Shung Chou, Li Hsueh Tsai
Yu-Chih Liang, Graduate Institute of Biomedical Technology, Taipei Medical University, Taipei, Taiwan, China
Hung-Jung Liu, Liang-Shung Chou, Li Hsueh Tsai, Department of Physiology, College of Medicine, Taipei Medical University, Taipei, Taiwan, China
Sheng-Hsuan Chen, Department of Internal Medicine, Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan, China
Chun-Chin Chen, Department of Internal Medicine, Min-Sheng Healthcare, Taoyuan, Taiwan, China
Author contributions: All authors contributed equally to the work.
Supported by the National Science Council of Taiwan (NSC 92-2320-B-038-027) and the Min-Sheng Healthcare (93MSH-TMU-006)
Correspondence to: Dr. Li Hsueh Tsai, Department of Physiology, Taipei Medical University, No. 250 Wu-Hsing Street, Taipei, Taiwan 11014, China. lhtsai@tmu.edu.tw
Telephone: +886-2-27361661-3181 Fax: +886-2-23781073
Received: May 27, 2004
Revised: May 28, 2004
Accepted: June 25, 2004
Published online: January 21, 2005
Abstract

AIM: To investigate the effect of lipopolysaccharide (LPS) on the diarrheogenic activity, gastrointestinal transit (GIT), and intestinal fluid content and the possible role of nitric oxide (NO) and prostaglandin E2 (PGE2) in gastrointestinal functions of endotoxin-treated mice.

METHODS: Diarrheogic activity, GIT, and intestinal fluid content as well as nitric oxide and PGE2 products were measured after intraperitoneal administration of LPS in mice.

RESULTS: LPS dose-dependently accumulated abundant fluid into the small intestine, induced diarrhea, but decreased the GIT. Both nitric oxide and PGE2 were found to increase in LPS-treated mice. Western blot analysis indicated that LPS significantly induced the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 in mice intestines. Pretreatment with NG-nitro-L-arginine-methyl ester (L-NAME, a non-selective NOS inhibitor) or indomethacin (an inhibitor of prostaglandin synthesis) significantly attenuated the effects of LPS on the diarrheogenic activity and intestine content, but reversed the GIT.

CONCLUSION: The present study suggests that the pathogenesis of LPS treatment may mediate the stimulatory effect of LPS on nitric oxide and PGE2 production and NO/prostaglandin pathway may play an important role on gastrointestinal function.

Keywords: Diarrhea; Gastrointestinal Transit; Lipopolysaccharide; Nitric Oxide; Prostaglandin E2