PMID- 19109869
OWN - NLM
STAT- MEDLINE
DCOM- 20090519
LR  - 20211025
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 14
IP  - 48
DP  - 2008 Dec 28
TI  - Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by 
      modulating inflammatory mediators.
PG  - 7353-60
AB  - 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-alpha (TNF-alpha), 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-kappaB (NF-kappaB) 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-alpha, 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-kappaB 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.
FAU - Yang, Tie-Cheng
AU  - Yang TC
AD  - 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.
FAU - Zhang, Shu-Wen
AU  - Zhang SW
FAU - Sun, Li-Na
AU  - Sun LN
FAU - Wang, Hong
AU  - Wang H
FAU - Ren, Ai-Min
AU  - Ren AM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lignans)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 001E35HGVF (magnolol)
RN  - 130068-27-8 (Interleukin-10)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/pharmacology/*therapeutic use
MH  - Biphenyl Compounds/pharmacology/*therapeutic use
MH  - Chemokine CCL2/metabolism
MH  - Disease Models, Animal
MH  - Gastrointestinal Diseases/*drug therapy/metabolism/*microbiology
MH  - Gastrointestinal Motility/drug effects
MH  - Ileum/metabolism
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-10/metabolism
MH  - Lignans/pharmacology/*therapeutic use
MH  - Lipopolysaccharides
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Sepsis/chemically induced/*complications/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC2778119
EDAT- 2008/12/26 09:00
MHDA- 2009/05/20 09:00
PMCR- 2008/12/28
CRDT- 2008/12/26 09:00
PHST- 2008/12/26 09:00 [entrez]
PHST- 2008/12/26 09:00 [pubmed]
PHST- 2009/05/20 09:00 [medline]
PHST- 2008/12/28 00:00 [pmc-release]
AID - 10.3748/wjg.14.7353 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2008 Dec 28;14(48):7353-60. doi: 10.3748/wjg.14.7353.