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目的研究银屑1号对咪喹莫特诱导小鼠银屑病模型血清中炎性因子IL-6,IL-17,INF-γ和角质形成细胞内核转录因子-κB(NF-κB)及NF-κB mRNA表达的影响。方法入选动物随机分为5组:正常组(Normal)、模型组(Model)、银屑1号高(HD)、中(MD)、低(LD)剂量组,除正常组外,所有小鼠外涂咪喹莫特软膏14日诱导为银屑病模型,银屑1号高、中、低剂量组给药剂量分别为50g/(kg·d),25g/(kg·d),12.5g/(kg·d),连续10d,正常组及模型组予等量生理盐水对照。检测表皮垂直厚度,血液蛋白芯片法检测血清I-L6,IL-17,INF-γ水平,苏木精-依红染色观察皮损组织结构改变,免疫组化法检测NF-κB含量,应用逆转录-聚合酶链反应检测NF-κB mRNA表达情况。结果与正常组比较,模型组角质增厚,镜下T淋巴细胞浸润明显,其炎性因子、NF-κB蛋白及基因表达均升高(P<0.01);同模型组比较,银屑1号高、中剂量组IL-6,IL-17,INF-γ水平下降明显(P<0.01);高、中、低剂量组表皮增厚程度明显降低(P<0.01),NF-κB蛋白水平明显降低(P<0.01),中、低剂量组NF-κB mRNA表达降低(P<0.05)。结论银屑1号对银屑病小鼠模型的角质增殖和炎性反应具有抑制作用,抑制NF-κB蛋白及基因的过度表达是其作用机制之一。
Objective To study the effect of psoriasis 1 on the expression of inflammatory factors IL-6, IL-17, INF-γ and keratinocyte nuclear factor-κB (NF-κB) and NF in keratinocytes induced by imiquimod -κB mRNA expression. Methods The animals were randomly divided into 5 groups: normal group, model group, psoriatic 1 (HD), middle (MD) and low (LD) The imipenem-ointment was orally administered on the 14th for the psoriasis model. The doses of the high, middle and low doses of the Pill No.1 were 50g / (kg · d), 25g / (kg · d), 12.5g / ( kg · d) for 10 days, the normal group and the model group were given the same amount of saline control. The thickness of epidermis was measured. The levels of serum IL-6, IL-17 and INF-γwere detected by blood protein chip method. The histological changes were observed by hematoxylin-eosin staining. The content of NF-κB was detected by immunohistochemistry The expression of NF-κB mRNA was detected by polymerase chain reaction. Results Compared with the normal group, the model group had thickening of keratinocytes, obvious infiltration of T lymphocytes and increased expression of inflammatory factors and NF-κB protein and gene (P <0.01). Compared with the model group, The levels of IL-6, IL-17 and INF-γincreased significantly in high and middle dose groups (P <0.01), while the levels of epidermal thickening in high, middle and low dose groups were significantly decreased (P <0.01) (P <0.01). The expression of NF-κB mRNA in the medium and low dose groups decreased (P <0.05). Conclusions Psoriasis 1 can inhibit the keratinocyte proliferation and inflammatory response in the mouse model of psoriasis. Inhibition of NF-κB protein and gene overexpression is one of its mechanisms.