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Nutrition Research and Practice ; : 3-10, 2015.
Artigo em Inglês | WPRIM | ID: wpr-105461

RESUMO

BACKGROUND/OBJECTIVES: Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. Previously, Sasa quelpaertensis leaves have been shown to mediate anti-inflammation and anti-cancer effects, although it remains unclear whether Sasa leaves are able to attenuate inflammation-related intestinal diseases. Therefore, the aim of this study was to investigate the anti-inflammatory effects of Sasa quelpaertensis leaf extract (SQE) using an in vitro co-culture model of the intestinal epithelial environment. MATERIALS/METHODS: An in vitro co-culture system was established that consisted of intestinal epithelial Caco-2 cells and RAW 264.7 macrophages. Treatment with lipopolysaccharide (LPS) was used to induce inflammation. RESULTS: Treatment with SQE significantly suppressed the secretion of LPS-induced nitric oxide (NO), prostaglandin E2 (PGE2), IL-6, and IL-1beta in co-cultured RAW 264.7 macrophages. In addition, expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and tumor necrosis factor (TNF)-alpha were down-regulated in response to inhibition of IkappaBalpha phosphorylation by SQE. Compared with two bioactive compounds that have previously been identified in SQE, tricin and P-coumaric acid, SQE exhibited the most effective anti-inflammatory properties. CONCLUSIONS: SQE exhibited intestinal anti-inflammatory activity by inhibiting various inflammatory mediators mediated through nuclear transcription factor kappa-B (NF-kB) activation. Thus, SQE has the potential to ameliorate inflammation-related diseases, including IBD, by limiting excessive production of pro-inflammatory mediators.


Assuntos
Humanos , Células CACO-2 , Técnicas de Cocultura , Colite Ulcerativa , Doença de Crohn , Dinoprostona , Trato Gastrointestinal , Inflamação , Doenças Inflamatórias Intestinais , Interleucina-6 , Enteropatias , Macrófagos , Óxido Nítrico , Óxido Nítrico Sintase Tipo II , Fosforilação , Prostaglandina-Endoperóxido Sintases , Sasa , Fatores de Transcrição , Fator de Necrose Tumoral alfa
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