徐长卿对溃疡性结肠炎模型大鼠核因子κB信号通路的影响

Effects of Cynanchum Paniculatum on NF-κB Signaling Pathway in Ulcerative Colitis Model Rats

目的:从炎症反应探讨徐长卿治疗溃疡性结肠炎(UC)的机制。方法:将60只雄性SD大鼠随机分为6组:正常组,模型组,柳氮磺吡啶组,徐长卿低、中、高剂量组。除正常组外,其余5组大鼠均以三硝基苯磺酸(TNBS)灌肠造模。灌肠24 h后,徐长卿低中高剂量组分别每天给予徐长卿0.4 g/kg、0.8 g/kg、1.6 g/kg体质量灌胃,柳氮磺吡啶组给予柳氮磺吡啶0.6 g/kg体质量灌胃,连续10 d。给药结束后,检测结肠组织髓过氧化物酶(MPO)、诱导型一氧化氮合酶(iNOS)活性,Western Blotting法检测磷酸化核因子κB抑制蛋白(p-IκBα)、胞质核因子κB(NF-κB)、胞核核因子κB蛋白水平。结果:徐长卿组较模型组MPO、iNOS活性显著降低(P<0.01),且随徐长卿剂量升高MPO、iNOS活性有降低趋势,但差异无统计学意义(P>0.05)。徐长卿组与模型组比较p-IκBα、胞核核因子水平显著降低(P<0.01),且随徐长卿剂量升高p-IκBα、胞核核因子κB水平有降低趋势(P>0.05)。徐长卿组与模型组比较胞质核因子κB水平显著升高(P<0.01),且随徐长卿剂量升高胞质核因子κB水平有升高趋势,但差异无统计学意义(P>0.05)。结论:徐长卿通过抑制核因子κB信号通路的激活,减少炎症介质的生成,是其治疗溃疡性结肠炎的可能机制。

Objective:To explore the mechanism of Cynanchum paniculatum in the treatment of ulcerative colitis.Methods:A total of 60 male SD rats were randomly divided into 6 groups:a normal group,a model group,a sulfasalazine group,a low,a medium and a high dose of Cynanchum paniculatum group.Except the normal group,TNBS enema was used in the other 5 groups.After 24 h of enema,the low,medium and high dose groups were given 0.4 g/kg,0.8 g/kg and 1.6 g/kg of Cynanchum paniculatum by gavage every day,and the sulfasalazine group was given 0.6 g/kg of sulfasalazine by gavage for 10 days.After administration,the activities of MPO and iNOS in colon tissue were detected,and p-IκBα,Cytoplasmic NF-κB,Nuclear NF-κB protein level was detected by Western Blotting.Results:the activities of MPO and iNOS in Cynanchum paniculatum group were significantly lower than those in model group(P<0.01),and the activities of MPO and iNOS decreased with the increase of Cynanchum paniculatum dose(P>0.05).Compared with the model group,the levels of p-IκBαand Cytoplasmic NF-κB of Cynanchum paniculatum group were significantly lower(P<0.01),and the levels of p-IκBα,Nuclear NF-κB decreased with the increase of the dosage of Cynanchum paniculatum(P>0.05).Compared with the model group,the level of cytoplasmic NF-κB in Cynanchum paniculatum group increased significantly(P<0.01),and the level of cytoplasmic NF-κB increased with the increase of the dose of Cynanchum paniculatum(P>0.05).Conclusion:The possible mechanism of Cynanchum paniculatum in treating ulcerative colitis is to inhibit the activation of NF-κB signaling pathway and reduce the production of inflammatory factors.