title: The anti-inflammation effect of baicalin on experimental colitis through inhibiting TLR4/NF-κB pathway activation.
abstract: BACKGROUND
  Baicalin holds a protective effect on inflammatory responses in several diseases. However, its molecular mechanism of anti-inflammatory activity on ulcerative colitis (UC) remains unknown. The present study was conducted to verify whether the anti-inflammation effect of baicalin on experimental colitis is via inhibiting TLR4/NF-κB pathway activation.
  
  
  METHODS
  The inflammatory response in RAW264.7 cells was induced by LPS and in rats by intrarectal administration of TNBS. Western blot analysis was carried out to examine toll-like receptor 4 (TLR4), NF-κB, p-NF-κB p65, IκB and p-IκB protein expressions in cells. Furthermore, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), cyclo-oxygenase-2 (Cox-2), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 levels in cell supernatant and rat serum were detected by appropriate kits. An immunohistochemical assay was applied to examine TNF-α and IL-1β protein expression in colon tissues and TLR4 and p-NF-κB p65 protein expressions in RAW264.7 cells.
  
  
  RESULTS
  Baicalin ameliorates the considered inflammatory symptoms of induced colitis. It could also down-regulate pro-inflammatory mediators in the colon mucosa. The decline in the production of pro-inflammatory cytokines was correlated with the decrease in mucosal TLR4 protein expression. The expression of p-NF-κB p65 protein was significantly decreased, which correlated with a similar decrease in p-IκB protein. Consistent with the in vivo results, baicalin blocked LPS-stimulated nuclear translocation of p-NF-κB p65 in mouse macrophage RAW264.7 cells.
  
  
  CONCLUSIONS
  The present study indicates for the first time that the mechanism for baicalin on abrogating experimental colitis was targeted inhibition of the TLR4/NF-κB pathway activation.
authors.affiliation: Key Laboratory of New Drug Delivery Systems of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Jiangsu, Nanjing 210028, PR China.
authors.forename: Li
authors.initials: L
authors.lastname: Cui
authors.affiliation: Key Laboratory of New Drug Delivery Systems of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Jiangsu, Nanjing 210028, PR China.
authors.forename: Liang
authors.initials: L
authors.lastname: Feng
authors.affiliation: Key Laboratory of New Drug Delivery Systems of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Jiangsu, Nanjing 210028, PR China.
authors.forename: Zhen Hai
authors.initials: ZH
authors.lastname: Zhang
authors.affiliation: Key Laboratory of New Drug Delivery Systems of Chinese Materia Medica, Jiangsu Provincial Academy of Chinese Medicine, Jiangsu, Nanjing 210028, PR China.
authors.forename: Xiao Bin
authors.initials: XB
authors.lastname: Jia
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage*; D002460:Cell Line; D018932:Chemokine CCL2 / Q000378:metabolism; D003093:Colitis, Ulcerative / Q000188:drug therapy* / Q000276:immunology; D003106:Colon / Q000187:drug effects* / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005419:Flavonoids / Q000008:administration & dosage*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016207:Cytokines; D005419:Flavonoids; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D018799:Intercellular Adhesion Molecule-1; C038044:baicalin
keywords: Baicalin; NF-κB; Pathway; TLR4; Ulcerative colitis