Department of Gastroenterology, Second Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Shanxi, China.
Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan, China.
Cell Prolif. 2019 Mar;52(2):e12547. doi: 10.1111/cpr.12547. Epub 2019 Jan 18.
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.
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.
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-1β, IL-6, Kc and TNF-α) compared with the control group. Meanwhile, NF-κB and Notch pathways were regulated.
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-κB and Notch signalling.
中药青黛汤（QBD）已被临床证明对治疗炎症性肠病（IBD）患者有效。然而，其作用机制尚不清楚。本研究旨在探讨 QBD 对溃疡性结肠炎小鼠模型的作用及其可能的机制。
C57/bL 小鼠给予 5% DSS 诱导结肠炎，并分为 QBD 组和柳氮磺胺吡啶组。每天记录体重、粪便和精神状态，处死小鼠后观察结肠组织病理学变化（杯状细胞等）。采用荧光素异硫氰酸酯-4000 检测反映肠黏膜通透性的变化。此外，还研究了细胞连接相关蛋白和可能的信号通路。
青黛汤能明显缓解炎症，其保护作用与柳氮磺胺吡啶灌肠组相当。结果发现，与对照组相比，QBD 治疗组的通透性显著降低，而柳氮磺胺吡啶组与 QBD 组之间无显著差异。QBD 治疗可上调紧密连接复合体（ZO-1、claudin-1 和 occludin）和 muc-2 的表达。与对照组相比，QBD 治疗组能显著减少促炎细胞因子（IL-1β、IL-6、KC 和 TNF-α）的产生和分泌。同时，NF-κB 和 Notch 信号通路也受到调节。
青黛汤能有效缓解结肠炎小鼠的肠道炎症和黏膜屏障功能障碍，其机制可能与抑制炎症级联反应以及通过 NF-κB 和 Notch 信号增强黏液层屏障和机械屏障功能有关。
