Dai Yan-Cheng, Zheng Lie, Zhang Ya-Li, Chen Xuan, Chen De-Liang, Wang Li-Juan, Tang Zhi-Peng
Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
World J Gastroenterol. 2017 Jul 14;23(26):4724-4734. doi: 10.3748/wjg.v23.i26.4724.
To investigate the underlying effect of Jianpi Qingchang decoction (JQD) regulating intestinal motility of dextran sulfate sodium (DSS)-induced colitis in mice.
C57BL/6 mice were randomly divided into four groups: the control group, the DSS group, the JQD group, and the 5-aminosalicylic acid group. Except for the control group, colitis was induced in other groups 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 day. The disease activity index, macroscopic and histopathologic lesions, and ultrastructure of colon interstitial cells of Cajal (ICC) were observed. The levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-10 and interferon gamma (IFN-γ), the expression of nuclear factor-kappa B (NF-κB) p65, c-kit, microtubule-associated protein 1 light chain 3 (LC3-II) and Beclin-l mRNA, and the colonic smooth muscle tension were assessed.
Acute inflammation occurred in the mice administered DSS. Compared with the control group, the levels of IL-1β, TNF-α, IL-10 and IFN-γ, the expression of LC3-II, Beclin-1 and NF-κB p65 mRNA, and the contractile frequency increased ( < 0.05), the expression of c-kit mRNA and the colonic smooth muscle contractile amplitude decreased in the DSS group ( < 0.05). Compared with the DSS group, the levels of IL-10 and IFN-γ, the expression of c-kit mRNA, and the colonic smooth muscle contractile amplitude increased ( < 0.05), the levels of TNF-α and IL-1β, the expression of LC3-II, Beclin-1 and NF-κB p65 mRNA, and the contractile frequency decreased in the JQD group ( < 0.05).
JQD can regulate the intestinal motility of DSS-induced colitis in mice through suppressing intestinal inflammatory cascade reaction, reducing autophagy of ICC, and regulating the network path of ICC/smooth muscle cells.
探讨健脾清肠汤（JQD）对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎肠道运动的潜在影响。
将C57BL/6小鼠随机分为四组：对照组、DSS组、JQD组和5-氨基水杨酸组。除对照组外，其他组通过给予含5%DSS的蒸馏水诱导结肠炎。造模7天后，小鼠灌胃给予相应药物。第15天处死小鼠。观察疾病活动指数、大体和组织病理学损伤以及结肠Cajal间质细胞（ICC）的超微结构。评估肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-10和干扰素γ（IFN-γ）水平、核因子-κB（NF-κB）p65、c-kit、微管相关蛋白1轻链3（LC3-II）和Beclin-1 mRNA的表达以及结肠平滑肌张力。
给予DSS的小鼠发生急性炎症。与对照组相比，DSS组IL-1β、TNF-α、IL-10和IFN-γ水平、LC3-II、Beclin-1和NF-κB p65 mRNA表达以及收缩频率增加（P<0.05），c-kit mRNA表达和结肠平滑肌收缩幅度降低（P<0.05）。与DSS组相比，JQD组IL-10和IFN-γ水平、c-kit mRNA表达和结肠平滑肌收缩幅度增加（P<0.05），TNF-α和IL-1β水平、LC3-II、Beclin-1和NF-κB p65 mRNA表达以及收缩频率降低（P<0.05）。
健脾清肠汤可通过抑制肠道炎症级联反应、减少ICC自噬以及调节ICC/平滑肌细胞网络通路来调节DSS诱导的小鼠结肠炎的肠道运动。
