| Berberine promotes recovery of colitis and inhibits inflammatory responses in colonic macrophages and epithelial cells in DSS-treated mice. | |
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MedLine Citation:
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PMID: 22173918 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Inflammatory bowel disease (IBD) results from dysregulation of intestinal mucosal immune responses to microflora in genetically susceptible hosts. A major challenge for IBD research is to develop new strategies for treating this disease. Berberine, an alkaloid derived from plants, is an alternative medicine for treating bacterial diarrhea and intestinal parasite infections. Recent studies suggest that berberine exerts several other beneficial effects, including inducing anti-inflammatory responses. This study determined the effect of berberine on treating dextran sulfate sodium (DSS)-induced intestinal injury and colitis in mice. Berberine was administered through gavage to mice with established DSS-induced intestinal injury and colitis. Clinical parameters, intestinal integrity, proinflammatory cytokine production, and signaling pathways in colonic macrophages and epithelial cells were determined. Berberine ameliorated DSS-induced body weight loss, myeloperoxidase activity, shortening of the colon, injury, and inflammation scores. DSS-upregulated proinflammatory cytokine levels in the colon, including TNF, IFN-γ, KC, and IL-17 were reduced by berberine. Berberine decreased DSS-induced disruption of barrier function and apoptosis in the colon epithelium. Furthermore, berberine inhibited proinflammatory cytokine production in colonic macrophages and epithelial cells in DSS-treated mice and promoted apoptosis of colonic macrophages. Activation of signaling pathways involved in stimulation of proinflammatory cytokine production, including MAPK and NF-κB, in colonic macrophages and epithelial cells from DSS-treated mice was decreased by berberine. In summary, berberine promotes recovery of DSS-induced colitis and exerts inhibitory effects on proinflammatory responses in colonic macrophages and epithelial cells. Thus berberine may represent a new therapeutic approach for treating gastrointestinal inflammatory disorders. |
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Authors:
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Fang Yan; Lihong Wang; Yan Shi; Hanwei Cao; Liping Liu; M Kay Washington; Rupesh Chaturvedi; Dawn A Israel; Hailong Cao; Bangmao Wang; Richard M Peek; Keith T Wilson; D Brent Polk |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-12-15 |
Journal Detail:
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Title: American journal of physiology. Gastrointestinal and liver physiology Volume: 302 ISSN: 1522-1547 ISO Abbreviation: Am. J. Physiol. Gastrointest. Liver Physiol. Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-02-22 Completed Date: 2012-04-16 Revised Date: 2012-05-23 |
Medline Journal Info:
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Nlm Unique ID: 100901227 Medline TA: Am J Physiol Gastrointest Liver Physiol Country: United States |
Other Details:
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Languages: eng Pagination: G504-14 Citation Subset: IM |
Affiliation:
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Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN, USA. fang.yan@vanderbilt.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects Berberine / therapeutic use* Colitis / chemically induced, drug therapy* Colon / cytology, physiopathology Cytokines / drug effects Dextran Sulfate Disease Models, Animal Epithelial Cells / physiology Inflammatory Bowel Diseases / drug therapy Macrophages / drug effects*, metabolism Mice Mice, Inbred C57BL Tumor Necrosis Factor-alpha / antagonists & inhibitors, biosynthesis |
| Grant Support | |
ID/Acronym/Agency:
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P01116087//PHS HHS; P30DK058404/DK/NIDDK NIH HHS; R01AT004821/AT/NCCAM NIH HHS; R01CA77955/CA/NCI NIH HHS; R01DK053620/DK/NIDDK NIH HHS; R01DK081134/DK/NIDDK NIH HHS; R01DK56008/DK/NIDDK NIH HHS; R01DK58587/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Tumor Necrosis Factor-alpha; 2086-83-1/Berberine; 9042-14-2/Dextran Sulfate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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