复方青黛颗粒对溃疡性结肠炎大鼠NF-κBP65、TNF-α表达的影响

Treatment with Compound Indigo Granules down-regulates NF-κB P65 and TNF-α expression in ulcerative colitis in rats

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.