Arvelexin inhibits colonic inflammation by suppression of NF-κB activation in dextran sulfate sodium-induced mice and TNF-α-induced colonic epithelial cells.
Recently, we reported the anti-inflammatory effects of arvelexin isolated from Brassica rapa in macrophages. In the present study, the effects of arvelexin were investigated in a dextran sulfate sodium (DSS)-induced colitis mouse model and in a cellular model. In the DSS-induced colitis model, arvelexin significantly reduced the severity of colitis, as assessed by disease activity, colonic damage, neutrophil infiltration, and levels of colonic iNOS. Moreover, arvelexin inhibited the expressions of IL-8, IP-10, ICAM-1, and VCAM-1 in HT-29 colonic epithelial cells. Arvelexin also inhibited the TNF-α-induced adhesion of U937 monocytic cells to HT-29 cells. Furthermore, arvelexin reduced p65 NF-κB subunit translocation to the nucleus and IκBα degradation in the colonic tissues and in TNF-α-induced HT-29 cells. These results demonstrate that the ameliorative effects of arvelexin on colonic injury are mainly related to its ability to inhibit the inflammatory responses via NF-κB inactivation, and support its possible therapeutic role in colitis.
Department of Pharmaceutical Biochemistry, College of Pharmacy, and ⊥Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University , Seoul, Korea.
Eu-Jin
EJ
Cho
Ji-Sun
JS
Shin
Kyung-Sook
KS
Chung
Yong Sup
YS
Lee
Young-Wuk
YW
Cho
Nam-In
NI
Baek
Hae-Gon
HG
Chung
Kyung-Tae
KT
Lee
D000818:Animals; D029741:Brassica rapa / Q000737:chemistry; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy; D003106:Colon / Q000166:cytology / Q000187:drug effects* / Q000503:physiopathology; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D019073:HT29 Cells; D006801:Humans; D020672:I-kappa B Proteins / Q000235:genetics / Q000378:metabolism; D007211:Indoles / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018517:Plant Roots / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D020298:U937 Cells; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D000094162:Phytoalexins
D016264:Dextran Sulfate; D020672:I-kappa B Proteins; D007211:Indoles; D018799:Intercellular Adhesion Molecule-1; D016209:Interleukin-8; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B; D052247:Nitric Oxide Synthase Type II; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C000606204:NFKBIA protein, human; C000606205:Nfkbia protein, mouse; C500823:arvelexin; D000094162:Phytoalexins; C496317:Nos2 protein, mouse