title: Curcumin improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the TLR4/NF-κB signaling pathway.
abstract: Curcumin is a widely used spice with anti-inflammatory and anticancer properties. It has been reported to have beneficial effects in experimental colitis. This study explored whether curcumin improves colonic inflammation in a rat colitis model through inhibition of the TLR4/NF-κB signaling pathway and IL-27 expression. After induction of colitis with 2,4,6-trinitrobenzene sulfonic acid, rats were intragastrically administered with curcumin or sulfasalazine daily for one week. Rat intestinal mucosa was collected for evaluation of the disease activity index, colonic mucosa damage index, and histological score. Myeloperoxidase activity was detected by immunohistochemistry, and mRNA and protein expression levels of TLR4, NF-κB, and IL-27 in colonic mucosa were detected by RT-PCR and Western blot. Compared with the untreated colitis group, the curcumin-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, NF-κB p65 protein, and IL-27 p28 protein (p < 0.05). TLR4 mRNA expression did not differ between groups. Disease activity index decreased more rapidly in the curcumin-treated group than in the sulfasalazine-treated group (p < 0.05). There was no significant difference in TLR4, NF-κB, and IL-27 mRNA and proteins between curcumin-treated and sulfasalazine-treated groups. Curcumin shows significant therapeutic effects on 2,4,6-trinitrobenzene sulfonic acid-induced colitis that are comparable to sulfasalazine. The anti-inflammatory actions of curcumin on colitis may involve inhibition of the TLR4/NF-κB signaling pathway and of IL-27 expression.
authors.affiliation: Department of Gastroenterology, The Western Hospital, First Affiliated Hospital of Guangxi Medical University, Nanning,Guangxi, China.
authors.forename: Zhaojing
authors.initials: Z
authors.lastname: Zeng
authors.forename: Lingling
authors.initials: L
authors.lastname: Zhan
authors.forename: Hui
authors.initials: H
authors.lastname: Liao
authors.forename: Lan
authors.initials: L
authors.lastname: Chen
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Lv
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D003474:Curcumin / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D005765:Gastrointestinal Agents / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D007378:Interleukins / Q000037:antagonists & inhibitors*; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D012460:Sulfasalazine / Q000494:pharmacology / Q000627:therapeutic use; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D014302:Trinitrobenzenesulfonic Acid / Q000009:adverse effects / Q000378:metabolism / Q000494:pharmacology
chemical_list: D000893:Anti-Inflammatory Agents; D005765:Gastrointestinal Agents; D007378:Interleukins; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D051996:Transcription Factor RelA; C556273:interleukin-27, rat; D012460:Sulfasalazine; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D003474:Curcumin