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目的探究复方蛹虫草(CCM)对葡聚糖硫酸钠(DSS)联合高脂诱导的溃疡性结肠炎(UC)的改善作用及初步机制。方法C57BL/6J雄性小鼠随机分为正常对照组、模型组、巴柳氮钠组及CCM 90、180和540 mg·kg~(-1)·d~(-1)组。采用DSS联合高脂饮食建立UC小鼠模型。造模同时ig给药,每天1次,连续8周,每周称量各组小鼠体质量,联苯胺法检测粪便隐血水平,酶联免疫吸附测定法(ELISA)测定血清细胞炎性因子TNF-α、IL-1β。HE染色法比较各组结肠组织病理改变,蛋白质免疫印迹(Western blot)方法检测结肠组织中IκB-α、NF-κBp65、TNF-α的表达。结果与正常组相比,模型组粪便隐血分数在第1、3、5、6周显著增加(P<0.05);小鼠结肠组织发生明显炎性细胞浸润(P<0.05);血清炎性因子TNF-α、IL-1β含量显著增高(P<0.01);结肠组织TNF-α、NF-κBp65表达显著增高(P<0.01),IκB-α表达显著降低(P<0.01)。与模型组相比,CCM组小鼠体质量均显著降低(P<0.05,P<0.01);CCM组小鼠粪便隐血显著减少(P<0.05);CCM高剂量组小鼠血清TNF-α显著降低(P<0.05),CCM中剂量组小鼠血清IL-1β显著降低(P<0.05);CCM中剂量组小鼠结肠组织炎性细胞浸润显著减少(P<0.05);CCM给药各组小鼠结肠组织TNF-α、NF-κBp65表达显著降低(P<0.01),IκB-α表达显著增高(P<0.01)。结论 CCM可以改善DSS联合高脂诱导的溃疡性结肠炎,其机制可能与其抑制NF-κB通路的激活有关。
Objective To investigate the effects of compound Cordyceps militaris (CCM) on dextran sulfate sodium (DSS) combined with hyperlipidemia-induced ulcerative colitis (UC) and its primary mechanism. Methods C57BL / 6J male mice were randomly divided into normal control group, model group, balsalazide group and CCM 90,180 and 540 mg · kg -1 · d -1 groups. The UC mice model was established by DSS combined with high-fat diet. At the same time, the rats were dosed once a day for 8 weeks. The body weight of each group was weighed every week, the concealed occult blood level was detected by the benzidine method, and the level of serum inflammatory cytokines TNF was measured by enzyme-linked immunosorbent assay (ELISA) -α, IL-1β. HE staining was used to compare the histopathological changes of colon tissues and the expressions of IκB-α, NF-κBp65 and TNF-α in colon tissues were detected by Western blot. Results Compared with the normal group, the fecal occult blood of the model group increased significantly (P <0.05) on the 1st, 3rd, 5th and 6th week. The inflammatory cell infiltration was found in the colon of the model group (P <0.05) TNF-α and IL-1β were significantly increased (P <0.01). The expressions of TNF-α and NF-κBp65 in colonic tissues were significantly increased (P <0.01) and the expression of IκB-α was significantly decreased (P <0.01). Compared with the model group, the body mass of CCM group was significantly lower (P <0.05, P <0.01); the occult blood of CCM group was significantly decreased (P <0.05); the serum level of TNF- (P <0.05). The serum level of IL-1β in the middle dose CCM group was significantly lower than that in the CCM group (P <0.05), and the inflammatory cell infiltration in the CCM middle dose group was significantly decreased The expression of TNF-α and NF-κBp65 in colonic tissue of mice was significantly decreased (P <0.01), and the expression of IκB-α was significantly increased (P <0.01). Conclusion CCM can improve the DSS combined with high-fat-induced ulcerative colitis, the mechanism may be related to its inhibition of NF-κB pathway activation.