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目的观察溃结灵对溃疡性结肠炎(UC)大鼠模型结肠黏膜核因子抑制蛋白-κB(IκB-α)基因表达及磷酸化核因子抑制蛋白-κB(pIκB-α)蛋白表达的作用,对其抗UC作用机制进行探讨。方法采用三硝基苯磺酸(TNBS)法复制UC大鼠模型并进行不同剂量药物干预。采用实时定量荧光PCR方法检测结肠黏膜IκB-α基因表达和Western blot方法检测结肠黏膜pIκB-α蛋白相对表达量。结果模型组IκB-α基因相对表达量明显低于正常组(P<0.01);溃结灵高剂量组IκB-α基因相对表达量明显高于模型组(P<0.05)。模型组pIκB-α蛋白相对表达量明显高于正常组(P<0.01);溃结灵低、高剂量组pIκB-α蛋白相对表达量均明显低于模型组(P<0.05)。结论溃结灵对TNBS法UC大鼠模型结肠黏膜IκB-α基因表达有上调作用及对pIκB-α蛋白表达有抑制作用,其抗UC作用的机理可能为抑制IκB-α的磷酸化,进而抑制IκB-α蛋白的降解,最终抑制核转录因子-κB的活化,减轻炎症反应。
Objective To observe the effect of Kuijie Ling on the expression of nuclear factor kappa B (IκB-α) gene and the expression of phosphorylated nuclear factor kappa B (α) in colonic mucosa of ulcerative colitis (UC) rats, Its anti-UC mechanism of action is discussed. Methods The rat model of UC was duplicated by trinitrobenzene sulfonic acid (TNBS) and the drug intervention was conducted at different doses. The expression of IκB-α in colonic mucosa was detected by real-time fluorescence quantitative PCR and the relative expression of pIκB-α in colonic mucosa was detected by Western blot. Results The relative expression of IκB-α in model group was significantly lower than that in normal group (P <0.01). The relative expression of IκB-α gene in high-dose Jiejiling group was significantly higher than that in model group (P <0.05). The relative expression level of pIκB-α in model group was significantly higher than that in normal group (P <0.01). The relative expression level of pIκB-α in low-dose and high-dose group was significantly lower than that in model group (P <0.05). Conclusion Kuijieling can up-regulate the expression of IκB-α in colonic mucosa and the expression of pIκB-α in UC rat model of TNBS, and its mechanism of anti-UC may be to inhibit the phosphorylation of IκB-α, IκB-α protein degradation, and ultimately inhibit the activation of nuclear factor-κB, reduce the inflammatory response.