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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 investigate the effect of Yin Dao I on the inflammatory pathway of nuclear factor-kappa B (NF-κB) induced by imiquimod (IMQ) in mice and its possible mechanism. Methods IMQ-induced mouse psoriasis model was established and randomly divided into model group, Psoriatic I group, tripterygium glycosides group, 10 mice in each group, 10 mice in normal control group as blank control group, blank control group and Model group was given the same amount of saline gavage I group, Tripterygium glycosides group were given silver I, Tripterygium glycosides gavage for 10 days, HE staining was observed in each group of mice lesion tissue morphology The expression of NF-κB p65 protein in skin lesions was detected by immunohistochemistry. The expression of NF-κB mRNA was detected by RT-PCR. The levels of serum interleukin 6 (IL-6), interleukin 10 interleukin 10 (IL-10), interleukin 17 (IL-17) and interferon gamma (INF-g) Results Compared with the blank control group, the model mice showed obvious erythema, scales and skin thickening. Compared with the model group, the levels of erythema, scaly and skin thickening of the mice in the Yin Dao I group and the tripterygium glycosides group were significantly reduced. The levels of IL-6, IL-10, IL (P <0.01). The expressions of NF-κB mRNA and NF-κB p65 also significantly decreased in Psoriatic I group and tripterygium glycosides group (all P <0.01). Conclusion Yin Dao I can significantly inhibit IMQ-induced mouse skin proliferation, which may be related to the inhibition of NF-κB gene expression and reduce the inflammatory response.