Basic Research
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Dec 28, 2008; 14(48): 7353-7360
Published online Dec 28, 2008. doi: 10.3748/wjg.14.7353
Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators
Tie-Cheng Yang, Shu-Wen Zhang, Li-Na Sun, Hong Wang, Ai-Min Ren
Tie-Cheng Yang, Shu-Wen Zhang, Hong Wang, Ai-Min Ren, Intensive Care Unit and Medical Department of Infection, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China
Li-Na Sun, Department of Pharmacology, School of Chemical Biology and Pharmaceutical Sciences, Capital Medical University, Beijing 100069, China
Author contributions: Zhang SW and Yang TC designed the research; Yang TC, Sun LN, Wang H and Ren AM performed the research; Yang TC and Sun LN analyzed data; Yang TC and Zhang SW wrote the paper.
Supported by Beijing Municipal Science & Technology Commission Major Sci-tech Program, No. H020920050130
Correspondence to: Shu-Wen Zhang, Professor, Intensive Care Unit and Medical Department of Infection, Beijing Friendship Hospital, Capital Medical University, No. 95, Yong An Road, Beijing 100050, China. zsw401106@sina.com
Telephone: +86-10-63138749 Fax: +86-10-62384167
Received: August 1, 2008
Revised: November 3, 2008
Accepted: November 10, 2008
Published online: December 28, 2008
Abstract

AIM: To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility.

METHODS: Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS). Male Wistar rats were randomly assigned to one of three treatment groups: magnolol prior to LPS injection (LPS/Mag group); vehicle prior to LPS injection (LPS/Veh group); vehicle prior to injection of saline (Control/Veh). Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), monocyte chemoattractant protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS) mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-κB (NF-κB) activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in the intestine 2 h after LPS injection.

RESULTS: Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPS-treated animals. TNF-α, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally, magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-κB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum.

CONCLUSION: Magnolol prevents sepsis-induced suppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.

Keywords: Sepsis; Motility; Cytokines; Magnolol; Lipopolysaccharide