Maggot protein ameliorates dextran sulphate sodium-induced ulcerative colitis in mice.
Maggot protein ameliorates dextran sulphate sodium-induced ulcerative colitis in mice.
复制标题
蛆蛋白可改善右旋糖酐硫酸钠诱导的小鼠溃疡性结肠炎。
DOI：
10.1042/bsr20181799
复制
发表时间：
2018
影响因子：
4
通讯作者：
Wang Yong
中科院分区：
文献类型：
--
作者：
Wang Rong;Wang Lei;Luo Yongzheng;Wang Daojuan;Du Ronghui;Du Jiancheng;Wang Yong
溃疡性结肠炎（Ulcerative colitis，UC）是一种常见的慢性缓解性疾病，但治疗效果不理想.蛆虫被称为传统中药，名为“五谷虫”。本研究的目的是研究蛆蛋白对葡聚糖硫酸钠（DSS）诱导的C57 BL/6小鼠结肠炎的治疗作用。本研究采用C57 BL/6雌性小鼠灌胃含3%DSS的无菌水建立UC模型。将小鼠随机分为5组：对照组（无菌水）、模型组（DSS）、治疗组（DSS +蛆虫蛋白）、美沙拉秦组（DSS +美沙拉秦）和蛆虫蛋白组（无菌水+蛆虫蛋白）。每天记录精神状态、排便特征和体重变化。疾病活动指数（DAI）作为疾病严重程度标准，根据体重和粪便稠度和出血计算。第12天处死所有小鼠。对结肠长度、结肠组织学改变和其他炎症因子进行分析和评价。结果表明，成功建立了小鼠结肠炎模型。与DSS模型组相比，蛆虫蛋白给药显著抑制UC的严重程度。此外，蛆蛋白有效地改善DSS诱导的体重减轻、结肠缩短和结肠组织学损伤。此外，蛆虫蛋白通过抑制核因子κB（NFκB）信号通路的激活发挥抗炎作用。总之，用蛆蛋白治疗不仅能够改善结肠炎的症状，而且能够改善患有DSS诱导的结肠炎的小鼠的微观炎症。本研究可能对开发炎症性肠病（IBD）的有效治疗策略具有意义。
Ulcerative colitis (UC) is a common chronic remitting disease but without satisfactory treatment. Maggots are known as a traditional Chinese medicine named as ‘wu gu chong’. The aim of the present study was to investigate the therapeutic effect of the maggot protein on dextran sulphate sodium (DSS)-induced colitis in C57BL/6 mice. In the present study, female C57BL/6 mice were given sterile water containing 3% DSS to establish the model of UC. Mice were randomly divided into five groups: control group (sterile water), model group (DSS), treatment group (DSS + maggot protein), mesalazine group (DSS + mesalazine), and maggot protein group (sterile water + maggot protein). The mental state, defecate traits, and changes in body weights were recorded daily. The disease activity index (DAI) as a disease severity criterion was calculated based on body weights and stool consistency and bleeding. All the mice were killed on the 12th day. Colon length, colon histological changes, and other inflammatory factors were analyzed and evaluated. The results showed that colitis models of mice were established successfully. Administration of maggot protein markedly suppressed the severity of UC compared with the DSS model group. Furthermore, maggot protein potently ameliorated DSS-induced weight loss, colon shortening, and colon histological injury. Moreover, the maggot protein exerted anti-inflammatory effects via inhibition of the activation of the nuclear factor κB (NFκB) signaling pathway. In summary, treatment by maggot protein was able to improve not only the symptoms of colitis, but also the microscopic inflammation in mice with DSS-induced colitis. The present study may have implications for developing an effective therapeutic strategy for inflammatory bowel diseases (IBDs).