肠炎康治疗DSS诱导小鼠实验性结肠炎的疗效及其机制研究  

Clinical Efficacy and Mechanism of Changyankang on DSS-Induced Colitis in Mice

作　　者：梁颖[1] 古筱茹[1] 刘俊娥[1] 姚晖[1] 成巧[1] 刁建新[2] 

机构地区：[1]南方医科大学附属佛山医院(佛山市第二人民医院)药学部,广东佛山528000 [2]南方医科大学中医药学院,广东广州510515

出　　处：《今日药学》2016年第5期321-324,共4页Pharmacy Today

摘　　要：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 efficacy and mechanism of Changyankang on DSS-induced colitis in mice.METHODS DSS-induced experimental colitis model in mice were induced and given Changyankang treatment with sulfasalazine enteric-coated tablets（ SASP） group as control. The inflammatory markers,the colon tissue disease,serum IL-1β,IL-2 levels and colon nuclear factor（ NF-κBp65） protein content were observed and compared. RESULTS Changyankang could significantly reduce colitis disease status of experimental colitis in mice,decrease serum IL-1β,IL-2 levels,reduce NF-κBp65 protein content（ P〈0.01）.CONCLUSION Changyankang has a good clinical efficacy on experimental colitis in mice,by inhibiting the expression and activation of NF-κBp65 mucosa and reduction of pro-inflammatory cytokine expression play a role.

关 键 词：溃疡性结肠炎 肠炎康 IL-1Β IL-2 NF-ΚBP65 

分 类 号：R97[医药卫生—药品]