QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling

QingBai decoction regulates intestinal permeability of dextran sulphate sodium-induced colitis through the modulation of notch and NF-κB signalling
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青白汤通过调节Notch和NF-κB信号调节右旋糖酐硫酸钠诱导的结肠炎肠道通透性

DOI:
10.1111/cpr.12547
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发表时间:
2019-03-01
期刊:
影响因子:
8.5
通讯作者:
Liang, Jie
Liang, Jie
中科院分区:
生物学1区
文献类型:
--
作者:
Lin, Jun-Chao;Wu, Jie-Qiong;Liang, Jie

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Objective Chinese Herb QingBai decoction (QBD) has been approved affective in the treatment of IBD patients in clinic. However, the underlying mechanism remains unknown. We aim to investigate the effect of QBD on the mouse model of ulcerative colitis and its possible mechanism. Methods C57/bL mice were given 5% DSS to induce colitis and were divided as QBD and mesalazine group. Weight, faeces and mental status were recorded each day and the histopathological changes (goblet cells etc) of the colon were observed after sacrificed. Fluorescein isothiocyanate-dextran 4000 was measured to reflect the intestinal mucosal permeability. In addition, cell junction-related proteins and possible signal pathways were investigated. Results QingBai decoction could significantly alleviate the inflammation and the protection effect of colitis is comparable as those in mesalazine enema group. It was found that the permeability reduced significantly with QBD treatment vs the control group, while no significant difference between the mesalazine and QBD groups. QBD treatment could upregulate the expression of tight junction complex(ZO-1, claudin-1 and occludin?and muc-2 expression. It significantly reduced the production and secretion of serials proinflammatory cytokines (IL-1 beta, IL-6, Kc and TNF-alpha) compared with the control group. Meanwhile, NF-kappa B and Notch pathways were regulated. Conclusion QingBai decoction can effectively alleviate intestinal inflammation and mucosal barrier function in colitis mice, and the mechanism may be related to the inhibition of inflammatory cascade as well as enhanced mucus layer barrier and mechanical barrier function by NF-kappa B and Notch signalling.