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目的:研究氧化苦参碱抗溃疡性结肠炎作用机制。方法:SPF级大鼠随机分成正常组、UC模型组、氧化苦参碱+UC模型组(ig给予氧化苦参碱180 mg·kg-1)、柳氮磺胺吡啶+UC模型组(ig给予柳氮磺胺吡啶600 mg·kg-1)。采用2,4,6-三硝基苯磺酸(TNBS)致大鼠溃疡性结肠炎症,连续给药21 d。实验结束后,剖取结肠病灶组织,采用免疫组织化学方法检测各组动物结肠组织细胞中核转录因子κB(NF-κB)的抑制蛋白(IκB-α)蛋白阳性细胞表达率,同时测定每组动物结肠组织中肿瘤坏死因子-α(TNF-α),白介素(interleukin,IL)1β(IL-1β),IL-6,IL-8细胞因子表达,并对每只动物结肠病理切片做显微镜检查。结果:氧化苦参碱组动物结肠黏膜细胞中IκB-α阳性细胞表达率21.8%±5.0%,显著低于模型组(25.6%±2.9%)(P<0.01);结肠细胞中TNF-α(66.23±2.64)pg·mg-1,IL-1β(149.42±64.69)pg·mg-1,IL-6(668.83±98.11)pg·mg-1和IL-8(91.83±23.14)pg·mg-14种细胞因子的表达率较模型组相比也显著降低(P<0.01);结肠组织显微镜检查,治疗组动物结肠细胞炎症、淋巴细胞浸润、黏膜损伤修复率明显高于模型组。结论:氧化苦参碱通过干预IκB-α蛋白表达,进而抑制溃疡性结肠炎症细胞中核转录因子κB(NF-κB)活性,产生抗炎效果。
Objective: To investigate the mechanism of oxymatrine against ulcerative colitis. Methods: SPF rats were randomly divided into normal group, UC model group, oxymatrine + UC model group (ig given oxymatrine 180 mg · kg -1), sulfasalazine + UC model group Sulfasalazine 600 mg kg-1). Rats with ulcerative colitis were induced with 2,4,6-trinitrobenzene sulfonic acid (TNBS) for 21 days. At the end of the experiment, the colon lesions were dissected and the expression of NF-κB positive cells was detected by immunohistochemical method in each group. At the same time, The expression of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), IL-6 and IL-8 in colonic tissues was examined. Results: The expression of IκB-α in colonic mucosa of oxymatrine group was 21.8% ± 5.0%, significantly lower than that in model group (25.6% ± 2.9%) (P <0.01) 66.23 ± 2.64) pg · mg-1, IL-1β (149.42 ± 64.69) pg · mg-1, IL-6 (668.83 ± 98.11) pg · mg-1 and IL-8 (91.83 ± 23.14) pg · mg- The expression of 14 kinds of cytokines was also significantly lower than that of the model group (P <0.01). The colonic tissue microscopy and colonic tissue inflammation, lymphocyte infiltration and mucosal injury in the treatment group were significantly higher than those in the untreated group. Conclusion: Oxymatrine can inhibit the activity of nuclear factor kappa B (NF-κB) in the inflammatory cells of the ulcerative colitis through the intervention of IκB-α protein.