抑瘤素M受体对慢性自身免疫性荨麻疹发病机制的影响  

Effect of Oncostatin M Receptor on the Pathogenesis of Chronic Autoimmune Urticaria

作　　者：陈贵婧 薄灵芳 尹晓华[1] 沙丹丹 张甜 Chen Guijing;Bo Lingfang;Yin Xiaohua;Sha Dandan;Zhang Tian(Hebei Traditional Chinese Medicine Hospital,Shijiazhuang,050000)

机构地区：[1]河北省中医院,石家庄050000

出　　处：《基因组学与应用生物学》2020年第2期737-745,共9页Genomics and Applied Biology

摘　　要：本研究旨在探讨抑瘤素M受体(OSMR)在慢性自身免疫性荨麻疹(CAU)发病机制中的作用。本研究分别检测30例CAU患者及30名健康受试者的皮肤组织中OSMR、JAK和STAT3的表达,研究显示OSMR、JAK和STAT3在CAU患者皮肤组织中高表达(p<0.05)。转染OSMR-siRNA可显著降低CAU模型小鼠血清炎症因子IL-1、IL-6和IFN-γ水平,而转染JAK/STAT3信号通路激动剂Tyr705则可显著升高炎症因子水平(p<0.05)。转染OSMR-siRNA可显著降低CAU小鼠瘙痒次数、瘙痒时间和嗜酸性粒细胞计数,而转染Tyr705则可显著升高CAU小鼠瘙痒次数、瘙痒时间和嗜酸性粒细胞计数(p<0.05)。转染OSMR-siRNA促进了CAU小鼠上皮细胞的增殖能力,并抑制了细胞凋亡(p<0.05)。而转染Tyr705则抑制了CAU小鼠上皮细胞的增殖能力,并促进了细胞凋亡(p<0.05)。转染OSMR-siRNA下调了上皮细胞中OSMR、JAK和STAT3的表达,而转染Tyr705则上调了OSMR、JAK和STAT3的表达(p<0.05)。总之,本研究表明OSMR基因在CAU患者皮肤组织中高表达。OSMR基因沉默可通过抑制JAK/STAT3信号通路来抑制炎症因子表达及嗜酸性粒细胞数量,促进上皮细胞增殖并抑制细胞凋亡。This aim of the study was to investigate the role of oncostatin M receptor(OSMR)in the pathogenesis of chronic autoimmune urticaria(CAU),respectively.The study examined the expression of OSMR,JAK and STAT3 in skin tissues of 30 CAU patients and 30 healthy subjects.The study showed that OSMR,JAK and STAT3 were highly expressed in skin tissues of patients with CAU(p<0.05).Transfection of OSMR-siRNA significantly reduced serum inflammatory cytokines IL-1,IL-6 and IFN-γlevels in CAU model mice,whereas transfection of JAK/STAT3 signaling pathway agonist Tyr705 significantly increased inflammatory factor levels(p<0.05).Transfection of OSMRsi RNA significantly reduced the number of itching,itching time and eosinophil count in CAU mice,while transfection of Tyr705 significantly increased the number of itching,itching time and eosinophil count in CAU mice(p<0.05).Transfection of OSMR-siRNA promoted the proliferation and inhibited apoptosis in CAU mouse epithelial cells(p<0.05).Transfection of Tyr705 inhibited the proliferation and promoted apoptosis in CAU mouse epithelial cells(p<0.05).Transfection of OSMR-siRNA down-regulated the expression of OSMR,JAK and STAT3 in epithelial cells,while transfection of Tyr705 up-regulated the expression of OSMR,JAK and STAT3(p<0.05).In conclusion,this study demonstrates that the OSMR gene is highly expressed in skin tissue of CAU patients.OSMR gene silencing inhibits the expression of inflammatory cytokines and eosinophils,promoting epithelial cell proliferation and inhibiting apoptosis,by inhibiting the JAK/STAT3 signaling pathway.

关 键 词：抑瘤素M受体 慢性自身免疫性荨麻疹 基因沉默 JAK/STAT3信号通路 炎症因子 

分 类 号：R758.24[医药卫生—皮肤病学与性病学]