Undaria pinnatifida attenuates DSS-Induced Colitis through Inhibition of NF-κB Activation in Mice
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Ulcerative colitis (UC) is a chronic gastrointestinal disorder, the symptoms of which include diarrhea, weight loss, abdominal pain, and intestinal bleeding, resulting in epithelial barrier disruption. Undaria pinnatifida (UP), one of brown algae family, exerts various beneficial biological property including preventing arteriosclerosis and menopausal disorders. This study aims to assess the mechanism by which UP acts a protective effect against dextran sodium sulfate (DSS)-induced colitis in vivo. Mice were divided into four groups : Group I-control group, Group II-DSS alone group, Group III-DSS+ UP (10 ㎎/㎏), Group IV-DSS + UP (100 ㎎/㎏). We evaluated the effects of UP on DSS-induced clinical symptoms by analyzing weight loss and colon length. The regulatory effects of UP on inflammatory mediators were determined in colitis tissue. Results showed that mice UP treatment significantly improved DSS-induced clinical symptoms including weight loss, colon length decrease and diarrhea. Additionally, UP attenuates DSS-induced inflammatory cytokine by blocking nuclear factor-κB (NF-κB) activation in the colons of colitis mice. Collectively, the findings of this study demonstrated the prospect of developing new agents from UP for UC treatment.
Abstract
Ulcerative colitis (UC) is a chronic gastrointestinal disorder, the symptoms of which include diarrhea, weight loss, abdominal pain, and intestinal bleeding, resulting in epithelial barrier disruption. Undaria pinnatifida (UP), one of brown algae family, exerts various beneficial biological property including preventing arteriosclerosis and menopausal disorders. This study aims to assess the mechanism by which UP acts a protective effect against dextran sodium sulfate (DSS)-induced colitis in vivo. Mice were divided into four groups : Group I-control group, Group II-DSS alone group, Group III-DSS+ UP (10 ㎎/㎏), Group IV-DSS + UP (100 ㎎/㎏). We evaluated the effects of UP on DSS-induced clinical symptoms by analyzing weight loss and colon length. The regulatory effects of UP on inflammatory mediators were determined in colitis tissue. Results showed that mice UP treatment significantly improved DSS-induced clinical symptoms including weight loss, colon length decrease and diarrhea. Additionally, UP attenuates DSS-induced inflammatory cytokine by blocking nuclear factor-κB (NF-κB) activation in the colons of colitis mice. Collectively, the findings of this study demonstrated the prospect of developing new agents from UP for UC treatment.
참고문헌 (29)
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