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目的:研究热瘀散对胃肠湿热型溃疡性结肠炎(ulcerative colitis,UC)模型大鼠的作用机制。方法:雄性SD大鼠52只,随机分为正常对照组、模型组、柳氮磺胺吡啶(SASP)组、热瘀散高剂量组及热瘀散低剂量组。采用复合因素(高脂、高糖饮食加湿热环境)复制胃肠湿热型模型,再用2,4,6-三硝基苯磺酸(TNBS)乙醇法复制UC模型。模型复制后各组大鼠给予相应药物治疗,连续15天,第16天处死,观察大鼠结肠黏膜损伤情况,并检测大鼠结肠组织髓过氧化物酶(MPO)活性。结果:模型组大鼠结肠黏膜大体评分、病理组织学变化表明模型复制成功;热瘀散能显著改善结肠黏膜的大体评分;热瘀散高、低剂量及SASP组均可降低大鼠肠组织MPO活性。结论:热瘀散具有降低MPO活性,抑制炎症效应细胞的增殖与活化,减少中性粒细胞浸润,从而减轻炎性反应、促进病变结肠溃疡的修复,对胃肠湿热型溃疡性结肠炎有明显的治疗作用。
Objective: To study the mechanism of heat-blood-stasis on gastrointestinal damp-heat ulcerative colitis (UC) model rats. Methods: Fifty-two male Sprague-Dawley rats were randomly divided into normal control group, model group, SASP group, high-dose heat-stasis powder group and low-dose heat stasis powder group. The gastrointestinal damp-heat model was duplicated by compound factors (high-fat and high-sugar diet humidified heat environment), then the UC model was duplicated by 2,4,6-trinitrobenzene sulfonic acid (TNBS) ethanol. After the model was replicated, the rats in each group were treated with the corresponding drugs for 15 consecutive days and sacrificed on the 16th day. The colonic mucosal injury in rats was observed, and the activity of myeloperoxidase (MPO) in the colon was detected. Results: The colonic mucosa of rats in the model group was generally graded, and the histopathological changes showed that the model was successfully replicated. Heat decoction could significantly improve the general score of colonic mucosa. Heat stasis, high dose, low dose and SASP group could reduce the MPO active. Conclusion: ReYu Powder can reduce the activity of MPO, inhibit the proliferation and activation of inflammatory cells, reduce the infiltration of neutrophils, thereby reducing the inflammatory reaction and promoting the healing of diseased colonic ulcers. It has obvious effects on gastrointestinal damp-heat ulcerative colitis Therapeutic effect.