Objective: Based on bioinformatics, gene set enrichment analysis (GSEA) and immune infiltration analysis were carried out on the microarray data of psoriasis expression profile to further understand the pathogenesis of psoriasis. Methods: GSE6710 chip data were obtained from gene expression database (GEO), and gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed using GSEA software. 22 kinds of immune cell gene expression matrices and R packages were downloaded from CIBERSOFT official website, and the immune cell infiltration matrix was obtained by R software and related graphs were drawn. Results: The pathways related to cell proliferation and innate immunity were highly expressed in psoriatic lesions, and some cancer-related pathways were highly expressed in psoriatic lesions. Immunized cell infiltration analysis showed that activated memory T cells, follicular helper T cells, M0 macrophages and activated dendritic cells were up-regulated in psoriatic skin lesion group, and inactive mast cells were down-regulated in psoriatic skin lesion group. Activated dendritic cells are positively correlated with follicular helper T cells, activated mast cells are positively correlated with M0 macrophages. Inactivated mast cells are negatively correlated with activated memory T cells, M1 macrophages are negatively correlated with regulatory T cells, M0 macrophages are negatively correlated with inactive mast cells. Conclusion: Cell proliferation and innate immunity are of great significance in the pathogenesis of psoriasis. Immune cell infiltration analysis is generally consistent with the current psoriasis pathogenesis model. Macrophages and mast cells also play a certain role in psoriasis.

目的 研究细胞分裂周期蛋白7(cdc7)在银屑病角质细胞增殖中的作用机制.方法 利用生物信息学方法分析cdc7在人银屑病皮损中的表达,并预测其转录因子结合位点;将Hacat细胞分为Hacat组、Hacat+白介素-22(IL-22)50 ng/mL组、Hacat+IL-22 100 ng/mL组、Hacat+IL-22 200 ng/mL组,应用 CCK8法、实时定量聚合酶链式反应(RT-qPCR)法检测各组细胞的增殖活性和cdc7的表达量;将小鼠随机分为对照组、模型组(咪喹莫特乳膏外涂建模),应用RT-qPCR法、免疫组化法检测各组小鼠cdc7表达量;将小鼠随机分为对照组、模型组、实验组(咪喹莫特乳膏外涂+cdc7抑制剂灌胃建模),每日观察皮损动态变化,并绘制银屑病面积与严重指数(PASI)趋势图.结果 cdc7在人银屑病皮损中高表达(P＜0.05),cdc7可能是作为信号转导和转录激活因子家族转录因子的下游靶点而发挥作用;Hacat组、Hacat+IL-22 50 ng/mL组、Hacat+IL-22 100 ng/mL组、Hacat+IL-22 200 ng/mL组细胞中 cdc7 mRNA表达量分别为(1.00±0.01)、(1.16±0.06)、(4.45±0.08)、(5.53±0.33)(F=139.300,P＜0.01),细胞增殖活性分别为(0.54±0.02)、(0.64±0.02)、(0.83±0.02)、(1.00±0.04)(F=176.600,P＜0.01).模型组小鼠 cdc7 mRNA 表达量(2.18±0.15)、cdc7细胞阳性率(21.10±0.46)％,显著高于对照组的(1.02±0.05)、(7.11±0.32)％,差异均有统计学意义(P＜0.01).与模型组比较,实验组小鼠背部皮损较轻,PASI评分上升较缓慢.结论 cdc7具有促进银屑病角质细胞增殖的作用.

目的:明确消银解毒饮通过细胞分裂周期蛋白7(cdc7)对小鼠银屑病模型角质细胞增殖的干预作用.方法:将20只健康雄性BALB/c小鼠随机分为对照组、银屑病模型组、消银解毒饮组与cdc7抑制剂TAK-931组,每组5只,除对照组外,每组背部涂抹咪喹莫特诱导银屑病模型,连续5天.对照组和银屑病模型组予蒸馏水10 mL/kg,消银解毒饮组和cdc7抑制剂TAK-931组小鼠分别予消银解毒饮23.4 g/kg,TAK-9312 mg/kg灌胃处理,每天2次,连续5天.每日观察皮损情况进行PASI评分;HE染色观察皮损组织形态学改变及表皮厚度;免疫组化法检测皮损表皮中cdc7表达.结果:银屑病模型建模成功.与银屑病模型组相比,消银解毒饮组与TAK-931组小鼠背部皮损PASI评分低,表皮增生程度较轻,炎性细胞浸润较少(均P<0.05);消银解毒饮组表皮cdc7阳性表达细胞较银屑病模型组明显减少(P<0.05).结论:消银解毒饮可能通过下调cdc7表达,抑制角质形成细胞的过度增殖,改善咪喹莫特诱导的小鼠银屑病样皮损.

Filter the best macroporous resin and establish purification technology of total flavonoids from the aerial part of Sonchus arvensis L.with the recovery index of total flavonoids as the reference.The best macroporous resin was filtered among the nine resins by investigating the static adsorption and desorption properties through experiments,and then optimize the separation process of total flavonoids from the aerial part of Sonchus arvensis L.by using the best resin.The results showed that the AB-8 macroporous resin had good adsorption and desorption.The optimal technological conditions were:pH =5.0,initial concentration 0.672 3 mg/mL,flow rate of adsorption 2 mL/min,2BV,70％ ethanol,and desorption flow rate 3 mL/min.The diameter height ratio of resin column was 1∶10 and the macroporous resin could be used under 3 times.Under this condition,the purity of total flavonoids had been increased from 1.61％ to 3.91％.The AB-8 macroporous resin could be used to purify the total flavonoids from the aerial part of Sonchus arvensis L.