Intestinal anti-inflammatory activity of Sasa quelpaertensis leaf extract by suppressing lipopolysaccharide-stimulated inflammatory mediators in intestinal epithelial Caco-2 cells co-cultured with RAW 264.7 macrophage cells.
- Author:
Kyung Mi KIM
1
;
Yoo Sun KIM
;
Ji Ye LIM
;
Soo Jin MIN
;
Hee Chul KO
;
Se Jae KIM
;
Yuri KIM
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: Sasa quelpaertensis; co-culture model; anti-inflammation; pro-inflammatory mediators
- MeSH: Caco-2 Cells*; Coculture Techniques; Colitis, Ulcerative; Crohn Disease; Dinoprostone; Gastrointestinal Tract; Humans; Inflammation; Inflammatory Bowel Diseases; Interleukin-6; Intestinal Diseases; Macrophages*; Nitric Oxide; Nitric Oxide Synthase Type II; Phosphorylation; Prostaglandin-Endoperoxide Synthases; Sasa*; Transcription Factors; Tumor Necrosis Factor-alpha
- From:Nutrition Research and Practice 2015;9(1):3-10
- CountryRepublic of Korea
- Language:English
- Abstract: 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.
