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作 者:杜立阳[1] 陈铭诗[1] 刘清芳[1] 程晓磊[1] 李鲜明[1]
机构地区:[1]中国医科大学附属第一医院中医科,辽宁省沈阳市110001
出 处:《世界华人消化杂志》2011年第12期1290-1294,共5页World Chinese Journal of Digestology
基 金:辽宁省自然科学基金资助项目;No.20092130~~
摘 要:目的:探讨复方青黛颗粒治疗溃疡性结肠炎(UC)大鼠的相关机制.方法:用三硝基苯磺酸(TNBS)法制备大鼠UC模型,分为空白对照组、模型对照组、柳氮磺吡啶(SASP)组、复方青黛颗粒低、中、高剂量组.造模后第3天开始灌胃给药,共给药10d,实验第14天,处死大鼠.取大鼠结肠组织及血清,用免疫组织化学SP法检测NF-κBP65蛋白表达,ELISA测定血清中肿瘤坏死因子α(TNF-α)的含量.结果:空白对照组与模型对照组比较,结肠组织中NF-κBP65蛋白表达及血清中TNF-α表达明显增高(0.276±0.0081vs0.138±0.003;67.657±3.580vs18.990±3.964,均P<0.05)复方青黛颗粒高剂量组与模型对照组相比,结肠组织中NF-κBP65蛋白表达及血清中TNF-α表达显著降低(0.217±0.007vs0.276±0.008;27.783±2.867vs67.657±3.580,均P<0.05).结论:复方青黛颗粒对TNBS诱导的UC大鼠的治疗作用可能与通过NF-κB信号传导通路调节TNF-α含量有关.AIM: To determine the mechanism underlyingthe therapeutic effects of Compound IndigoGranules (CIG) against ulcerative colitis by investigating the effect of treatment with CIG on the expression of nuclear factor-κB P65 (NF-κB P65) and tumor necrosis factor (TNF)-α in the colon of rats with experimental ulcerative colitis.METHODS: Ulcerative colitis was induced in rats with trinitrobenzenesulfonic acid (TNBS). Rats were divided into control group, model group, salazosulfapyridine (SASP) group, low-,medium-, and high-dose CIG groups. Except the control group, the other groups were intragastrically given normal saline, SASP, and different doses of CIG from day 3 after model induction for 10 days, respectively. On day 14, all rats were killed to take colon and serum samples for measuring colonic NF-κB P65 expression by immunohistochemisty and serum TNF-α levels by enzyme-linked immunosorbent assay (ELISA).RESULTS: The levels of NF-κB P65 protein expression in the colon and serum TNF-α were signifi cantly higher in the model group than in the control group (0.138 ± 0.003 vs 0.276 ± 0.0081; 18.990 ± 3.964 vs 67.657 ± 3.580, both P 0.05) but were significantly lower in the high-dose CIG group than in the model group (0.217 ± 0.007 vs 0.276 ± 0.008; 27.783 ± 2.867 vs 67.657 ± 3.580, both P 0.05).CONCLUSION: Treatment with CIG significantly decreased the levels of NF-κB P65 protein expression in the colon and serum TNF-α in rats with ulcerative colitis. CIG exerts therapeutic effects against ulcerative colitis possibly via mechanisms associated with the NF-κB signaling pathway and down-regulation of TNF-α.
关 键 词:复方青黛颗粒 溃疡性结肠炎模型大鼠 NF-ΚBP65 肿瘤坏死因子Α
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