Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium- Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-kappa B Activation

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	Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium- Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-kappa B Activation
	Li, Juan ; Zhong, Wei ; Wang, Weiwei ; Hu, Shaoping ; Yuan, Jiahui ; Zhang, Bing ; Hu, Tianhui ; Song, Gang ; Li J(李娟) ; Zhang B(张兵) ; Hu TH(胡天惠) ; Song G(宋刚)
刊名	http://dx.doi.org/10.1371/journal.pone.0087810
	2014-02-04
关键词	BOWEL-DISEASE INTESTINAL METABOLITE CELLS ACCUMULATION MECHANISMS GROWTH CANCER APOPTOSIS BACTERIA PATHWAY
英文摘要	National Natural Science Foundation of China [31071187, 81172284, 81272721]; Fundamental Research Funds for the Central Universities [2010121102]; Xiamen Municipal Science and Technology Innovation Fund Project [3502Z20114018]; Program for New Century Excellent Talents in Fujian Province University; Phytogenic compounds with anti-oxidant and anti-inflammatory properties, such as ginsenoside metabolite compound K (CK) or berberine (BBR), are currently discussed as promising complementary agents in the prevention and treatment of cancer and inflammation. The latest study showed that ginsenoside Rb1 and its metabolites could inhibit TNBS-induced colitis injury. However, the functional mechanisms of anti-inflammation effects of ginsenoside, particularly its metabolite CK are still not clear. Here, using dextran sulfate sodium (DSS)-induced colitis in mice, clinical parameters, intestinal integrity, pro-inflammatory cytokines production, and signaling pathways in colonic tissues were determined. In mild and sever colitis mice, CK and BBR (as a positive agent) alleviated colitis histopathology injury, ameliorated myeloperoxidase (MPO) activity, reduced pro-inflammatory cytokines production, such as, IL-6, IL-1 beta, TNF-alpha, and increased anti-inflammatory cytokine IL-10 production in both mice colon tissues and blood. Nevertheless, the results revealed that CK and BBR inhibited NF-kappa B p65 nuclear translocation, downregulated p-I kappa B alpha and upregulated I kappa B alpha, indicating that CK, as well as BBR, suppressed the activation of the NF-kappa B pathway in the progression of colitis with immunofluorescence, immunohistochemical and western blotting analysis. Furthermore, CK inhibited pro-inflammatory cytokines production in LPS-activated macrophages via down-regulation of NF-kappa B signaling pathway. Taken together, our results not only reveal that CK promotes the recovery of the progression of colitis and inhibits the inflammatory responses by suppressing NF-kappa B activation, but also suggest that CK downregulates intestinal inflammation through regulating the activation of macrophages and pro-inflammatory cytokines production.
语种	英语
出版者	PUBLIC LIBRARY SCIENCE
内容类型	期刊论文
源URL	[http://dspace.xmu.edu.cn/handle/2288/93668]
专题	医学院－已发表论文
推荐引用方式 GB/T 7714	Li, Juan,Zhong, Wei,Wang, Weiwei,et al. Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium- Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-kappa B Activation[J]. http://dx.doi.org/10.1371/journal.pone.0087810,2014.
APA	Li, Juan.,Zhong, Wei.,Wang, Weiwei.,Hu, Shaoping.,Yuan, Jiahui.,...&宋刚.(2014).Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium- Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-kappa B Activation.http://dx.doi.org/10.1371/journal.pone.0087810.
MLA	Li, Juan,et al."Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium- Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-kappa B Activation".http://dx.doi.org/10.1371/journal.pone.0087810 (2014).