Anti-inflammatory effects of Retama monosperma in acute ulcerative colitis in rats.
Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, is a chronic intestinal disorder resultant from a dysfunctional epithelial, innate and adaptive immune response to intestinal microorganisms. Current IBD treatment presents limitations in both efficacy and safety that stimulated for new active drugs. Retama spp. have been traditionally used in the Mediterranean region in treatment of pain and inflammation. In this study, the anti-inflammatory and protective properties of a standardised aqueous extract from Retama monosperma (RmE) was evaluated in vivo, by intra-colonic administration of trinitrobenzene sulfonic acid (TNBS) in rats as a Crohn's disease model. The qualitative and quantitative analysis of flavonoids from RmE was performed by high-performance liquid chromatography-tandem mass spectrometry. Oral administration of RmE diminished the severity and extension of the intestinal injuries induced by TNBS. In addition, RmE increased mucus production in goblet cells in colon mucosa, decreased neutrophil infiltration and cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) overexpression. Similarly, RmE significantly reduced p38 mitogen-activated protein kinase activation, preventing the inhibitory protein IκB degradation in colonic mucosa. RmE anti-inflammatory effects seem to be related to impairment of neutrophil function and COX-2 and iNOS down-regulation possibly through p38 MAPK and nuclear transcription factor kappa B signalling pathways. These results suggest that RmE might contribute to the development of new pharmaceutical products for inflammatory bowel disease.
Department of Pharmacology, Faculty of Pharmacy, University of Seville, Seville, Spain.
Haidee
H
González-Mauraza
Carmen
C
Martín-Cordero
Catalina
C
Alarcón-de-la-Lastra
M Angeles
MA
Rosillo
Antonio J
AJ
León-González
Marina
M
Sánchez-Hidalgo
D000208:Acute Disease; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D003106:Colon / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004353:Drug Evaluation, Preclinical; D000431:Ethanol; D007887:Fabaceae / Q000737:chemistry*; D015870:Gene Expression; D020672:I-kappa B Proteins / Q000235:genetics / Q000378:metabolism; D020935:MAP Kinase Signaling System; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid
D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D016328:NF-kappa B; D010936:Plant Extracts; D000431:Ethanol; D014302:Trinitrobenzenesulfonic Acid; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat