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目的探讨肠炎康对葡聚糖硫酸钠(dextran sulfate sodium,DSS)致实验性小鼠结肠炎模型(ulcerative colitis,UC)的治疗作用及机制。方法采用DSS诱导实验性小鼠结肠炎模型,给予肠炎康治疗,并与柳氮磺吡啶肠溶片(SASP)组做对照,观察并比较各组小鼠的结肠炎炎症指标,结肠组织病理学变化、血清中IL-1β、IL-2水平及结肠组织核因子(NF-κBp65)的蛋白含量。结果肠炎康可显著减轻实验性结肠炎小鼠的结肠炎症状态,降低血清IL-1β、IL-2水平,降低NF-κBp65蛋白含量(P均<0.01)。结论肠炎康对实验性结肠炎小鼠有很好的临床疗效,作用机制可能通过抑制肠黏膜NF-κBp65的活化表达,下调促炎性细胞因子表达发挥作用。
Objective To investigate the therapeutic effect and mechanism of Changyankang on dextran sulfate sodium (DSS) -induced experimental mouse colitis model (UC). Methods The model of colitis induced by DSS was induced in rats. The rats were treated with Changyankang and compared with the SASP group. The colitis index, colonic histopathology Changes in serum IL-1β, IL-2 levels and colon tissue nuclear factor (NF-κBp65) protein content. Results Enteric Kang can significantly reduce colitis in experimental colitis mice, lower serum IL-1β, IL-2 levels, lower NF-κB p65 protein content (P all <0.01). Conclusion: Yan Yan Kang in experimental colitis mice have a good clinical effect, the mechanism may inhibit the activation of intestinal mucosal expression of NF-κBp65, down-regulated proinflammatory cytokines play a role.