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目的观察DPP-4抑制剂Alogliptin对三硝基苯磺酸诱导的溃疡性结肠炎模型小鼠结肠的MPO值,血清IL-8、TNF-α和GLP-2水平的影响,并探讨Alogliptin对炎症性肠病(IBD)的治疗机制。方法雄性BALB/c小鼠48只,分为6组,每组8只,分别为正常对照组、模型组、柳氮磺吡啶治疗组(520 mg/kg),Alogliptin高、中、低剂量组(1、0.3、0.1mg/kg)。模型组采用三硝基苯磺酸(TNBS)对BALB/c小鼠进行灌肠,制作溃疡性结肠炎小鼠模型,经灌胃给予药物治疗后,观察DPP-4酶抑制剂Alogliptin对肠炎小鼠腹泻,组织形态损伤,结肠组织MPO酶活力,血清IL-8、TNF-α和GLP-2含量的影响。结果与模型组相比,Alogliptin高、中剂量组能够改善肠炎小鼠临床症状,减轻结肠黏膜损伤,显著降低TNBS诱导的溃疡性结肠炎小鼠的DAI评分(P<0.01),并且治疗组小鼠结肠组织MPO酶活性、血清IL-8和TNF-α的浓度较模型组显著降低(P<0.05);而Alogliptin治疗组小鼠血清GLP-2的含量较模型组和正常组都有显著升高(P<0.05)。结论 DPP-4酶抑制剂Alogliptin能够有效抑制小鼠肠道炎性细胞的浸润,减轻肠黏膜的病理性损伤,对TNBS诱导的肠炎小鼠具有显著的治疗作用。
Objective To observe the effects of DPP-4 inhibitor Alogliptin on the colonic mucosal MPO, serum IL-8, TNF-α and GLP-2 levels in TNBS-induced mouse models of ulcerative colitis and to explore the effect of Alogliptin on inflammation Treatment of bowel disease (IBD). Methods Forty eight male BALB / c mice were randomly divided into 6 groups (n = 8, n = 8): normal control group, model group, sulfasalazine treatment group (520 mg / kg), Alogliptin high, (1, 0.3, 0.1 mg / kg). The model group was treated with trinitrobenzene sulfonic acid (TNBS) to enema the BALB / c mice to make the ulcerative colitis mouse model. After gavage and drug treatment, the effect of DPP-4 enzyme inhibitor Alogliptin on enteritis mice Diarrhea, histopathological damage, MPO activity in colonic tissue, serum levels of IL-8, TNF-α and GLP-2. Results Compared with the model group, Alogliptin high and middle dose groups could improve the clinical symptoms, reduce colonic mucosal injury, significantly reduce the DAI scores in TNBS-induced ulcerative colitis mice (P <0.01), and the treatment group was smaller Compared with model group, the concentration of MPO and serum IL-8 and TNF-α in murine colon tissue significantly decreased (P <0.05), while the level of GLP-2 in Alogliptin treated group was significantly higher than that of model group and normal group High (P <0.05). Conclusion DPP-4 enzyme inhibitor Alogliptin can effectively inhibit intestinal inflammatory cell infiltration in mice and relieve the pathological damage of intestinal mucosa, and has a significant therapeutic effect on TNBS-induced enteritis mice.