Arvelexin inhibits colonic inflammation by suppression of NF-κB activation in dextran sulfate sodium-induced mice and TNF-α-induced colonic epithelial cells

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[1] Cho, Eu-Jin
[2] 1,3,Shin, Ji-Sun
[3] 1,Chung, Kyung-Sook
[4] Lee, Yong Sup
[5] 3,Cho, Young-Wuk
[6] Baek, Nam-In
[7] Chung, Hae-Gon
[8] 1,Lee, Kyung-Tae
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Lee, K.-T. (ktlee@khu.ac.kr) | 1600年 / American Chemical Society卷 / 60期
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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. © 2012 American Chemical Society;
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