健脾清肠方对DSS诱导结肠炎小鼠肠道动力学影响的研究  

Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium induced colitis in mice

作　　者：戴彦成[1] 郑烈[1] 张亚利[1] 陈璇[1] 陈得良[1] 戴悦婷 唐志鹏[1] 

机构地区：[1]上海中医药大学附属龙华医院消化内科,上海中医药大学脾胃病研究所,上海200032

出　　处：《中国中西医结合消化杂志》2017年第2期123-128,共6页Chinese Journal of Integrated Traditional and Western Medicine on Digestion

基　　金：国家自然科学基金(No:81403355,81573892);上海市中医药新三年行动计划项目(No:ZY3-RCPY-2-2001)

摘　　要：[目的]探讨健脾清肠方(JQD)对DSS诱导结肠炎小鼠肠道动力的作用机制。[方法]C57BL/6小鼠随机分为Control组、DSS组、JQD组、5-ASA组。除Control组外,余各组小鼠用5%DSS自由饮用诱导结肠炎模型,造模7d后灌胃给药。第15天处死小鼠收集结肠组织,检测结肠组织病理学,ICC的超微结构,结肠组织IL-1β、IL-10、IFN-γ、TNF-α含量,c-kit mRNA、LC3-II mRNA、Beclin-l mRNA、NF-κB p65表达和结肠平滑肌张力。[结果]与DSS组比较,JQD组结肠黏膜表面上皮细胞移行修复,少量炎症细胞浸润,黏膜腺体基本恢复正常;ICC与其他细胞间连接完好,内部细胞器结构相对完整,可见到少量自噬泡存在;结肠组织IL-1β、TNF-α含量降低,IL-10、IFN-γ含量上升;c-kit mRNA表达上调,LC-3II mRNA、Beclin-1mRNA、NF-κB p65表达下降;结肠平滑肌条收缩振幅上升、收缩频率减少。[结论]JQD调节DSS模型小鼠异常肠道动力,其机制可能是通过抑制NF-κB/TNF-α通路及调节细胞因子IL-1β、IL-10、IFN-γ表达,抑制了肠道炎症的级联放大反应;抑制ICC过度自噬,调控ICC/SMC网络通路。[Objective]This study was aimed to explore the mechanism underlying regulatory effect of Jianpi Qingchang decoction（JQD）on intestinal motility of DSS-induced colitis in mice. [Methods]C57BL/6 mice were randomly divided into four groups：the control group,the DSS group,the JQD group, and the 5- ASA group. Except the control group, colitis was induced by giving distilled water containing 5% DSS. Seven days after modeling,the mice were administered corresponding drugs intragastrically. The mice were sacrificed on the 15 th day. The histopathologic lesions, and ultrastructure of colon ICC were ob- served. The levels of TNF-α, IL-1β, IL-10, IFN-7, the expression of NF-kB p65, c-kit mRNA, LC3-II mR- NA,Beclin-1 mRNA, and the colonic smooth muscle tension were assessed. [Results]Compared with the DSS group,the colons presented the migration and repair of epithelial ceils on the erosive mucosal surface with infiltration of fewer inflammatory cells and recovery of the glandular structure in the JQD group. The configuration of ICC was normal with intact connections between cells,and the ridge of mitochondria and a few autophagic vacuoles existed. The IL-1β and TNF-α levels decreased; IL-10 and IFN-7 levels in-creased. C-kit mRNA expression increased;LC-3II mRNA,Beclin-1 mRNA and NF-kB p65 expression de- creased. The colonic smooth muscle contractile amplitude increased,and the contractile frequency decreased in the JQD group. EConelusion]JQD can regulate the intestinal motility involved in inhibiting the NF-kB/ TNF-α pathway, regulating IL-113, IL-10, and IFN-T expression, suppressing intestinal inflammatory cascade reaction,inhibiting excessive autophagy of ICC,and regulating the network path of ICC/SMC.

关 键 词：溃疡性结肠炎 健脾清肠方 肠道动力 CAJAL间质细胞 

分 类 号：R285.5[医药卫生—中药学]