银屑I号对咪喹莫特诱导小鼠银屑病模型核转录因子-κB的调控作用及机制

Effects of Yinxieyihao on Nuclear Factor Kappa B for Imiquimod Induced Psoriasis Mice Model

目的观察银屑I号对咪喹莫特(imiquimod,IMQ)诱导小鼠银屑病模型核转录因子-κB(nuclear factor,NF-κB)炎症通路的影响及其可能的作用机制。方法建立IMQ诱导小鼠银屑病模型,随机分为模型组、银屑I号组、雷公藤多甙组,每组10只,另选正常小鼠10只作为空白对照组,空白对照组及模型组予等量生理盐水灌胃,银屑I号组、雷公藤多甙组分别给予银屑I号、雷公藤多甙灌胃,连续10天,HE染色观察各组小鼠皮损组织形态学变化;免疫组化法检测皮损组织NF-κB p65蛋白水平,RT-PCR法检测NF-κB mRNA表达情况,订制血液蛋白芯片检测血清白介素6(interleukin 6,IL-6)、白介素10(interleukin 10,IL-10)、白介素17(interleukin 17,IL-17)、干扰素γ(interferon gamma,INF-g)含量。结果与空白对照组比较,模型组小鼠出现明显的红斑、鳞屑及皮肤增厚。与模型组比较,银屑I号组、雷公藤多甙组小鼠红斑、鳞屑及皮肤增厚程度明显减轻;银屑I号组、雷公藤多甙组血清IL-6、IL-10、IL-17、INF-γ水平明显降低(P均<0.01);银屑I号组、雷公藤多甙组皮损组织NF-κB mRNA、NF-κB p65表达也明显降低(P均<0.01)。结论银屑I号能够明显抑制IMQ诱导小鼠模型皮肤增殖,这可能与抑制NF-κB基因表达及减轻炎症反应有关。

Objective To observe the effects of YinXieYiHao （YXIH） on nuclear factor （NF） kappa B inflammatory pathway for imiquimod （ IMQ ） induced psoriasis mice model and analysis it＇ s possible therapeutic rneehanism. Methods IMQ induced psoriasis mice mode/were conducted,which were randomly divided into model group（ MP）, YXIH group（YXYHP） , tripterygium glycosides group（ TGP）, another 10 mice were divided into blank control group（BCP）. Corresponding lavage method were employed for teen days. RT-PCR and IHC were applied to deteete protein and gene expression level of NF-κB in mice skin issue. HE staining were em ployed to observe the histological changes of mice skin issue. We detected IL-6, IL-10, IL-17, INF-g level of peripheral blood. Results MP appeared obvious erythema, scales and thickening of the skin; Compared with BCP, erythema, scales and skin thickened of other groups were significantly reduce; Compared with MP, IL-6, IL-10, 1L-17,INF-g level of peripheral blood were significantly decreased in YXYHP,TGP （all P 〈 0.01 ）. Compared with MP, expression of NF-κBmRNA in YXYHP,TGP were obviously declined （ all P 〈 0.01 ）, so was the expression of NF-KB p65. Conclusion YXIH could reduce inflammatory response of psoriasis mice model, the mechanism of which may be associated with the inhibition of NF-κB expression.