苦参素对溃疡性结肠炎的治疗作用机理研究

Mechanism of Kushenin treating ulcerative colitis by interventing IκB-α protein

目的研究苦参素抗溃疡性结肠炎作用机理。方法 SPF级大鼠随机分成正常组、UC模型组、苦参素+UC模型组、柳氮磺胺吡啶+UC模型组,苦参素和柳氮磺胺吡啶以灌胃方式给药。采用免疫组织化学方法检测各组动物结肠组织细胞中IκB-α蛋白阳性细胞表达率,同时测定每组动物结肠组织中TNF-α、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。结果苦参素组和柳氮磺胺吡啶组动物结肠粘膜细胞中IκB-α蛋白阳性细胞表达率显著低于模型组(P<0.01);与模型组相比,治疗组动物结肠细胞中TNF-α、IL-1β,IL-6和IL-8四种细胞因子的表达率也显著降低(P<0.05);苦参素具有极显著性(P<0.01)。从结肠组织显微镜检查图片上看,治疗组动物结肠细胞炎症、淋巴细胞浸润、粘膜损伤修复率明显高于模型组。结论苦参素通过干预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(nuclear transcription factor-kappaB,NF-κB)活性,产生抗炎效果。

Objective To study the mechanism of Kushenin treating rats ulcer colitis. Methods SPF rats were randomly divided into normal group UC model group Kushenin＋UC group,sulfasalazine ＋UC model group,Kushenin and sulfasalazine were given by ig method. Immunohistochemistry was used to detect IκB-α protein in colon tissue cells of animals, while TNF- α ,IL-1β ,IL-6,IL-8 cytokines were measured in each colonic tissue ,and microscopic examination of colonic biopsy were done. Results IκB-α protein expressions of animals colonic mucosa of Kushenin group and the sulfasalazine group were significantly lower than model group （P〈0.01）.Compared with model group, the TNF-α, IL-1β,IL-6 and IL-8 four kinds of cytokine expressions were significantly lower（P〈0.05 ）. Kushenin had a extremely significant（P〈0.01 ）. Microscopic examination of colon tissue from the picture show that the colonic inflammation, lymphocyte infiltration, mueosal damage of treatment group were significantly better than the model group. Conclusion Kushenin has anti-inflammatory effect by interfering with the IκB-α protein expression, and inhibit the nuclear transcription factor KB （nuclear transcription factor-kappaB, NF-KB）activity in colitiscell.