哮喘豚鼠肺组织中的CARM1和NF-κB表达及地塞米松的干预作用  

Expression of CARM1 and NF-κB in Asthmatic Guinea Pigs and Interference Effect of Dexamethason

作　　者：王翠莲[1] 刘泉[2] 傅恩清[2] 金发光[2] 楚东岭[2] 

机构地区：[1]苏州高新区人民医院呼吸科,江苏苏州215129 [2]第四军医大学唐都医院呼吸科,陕西西安710038

出　　处：《现代生物医学进展》2011年第24期4834-4836,共3页Progress in Modern Biomedicine

摘　　要：目的:探讨豚鼠支气管哮喘模型中共激活因子相关的精氨酸甲基转移酶1(coactivator-associated arginine methyltransferase1,CARM1)和核因子-B(NF-B)在气道和肺组织的表达变化及地塞米松的干预作用。方法:36只白色雄性豚鼠随机分为正常对照组、哮喘组和地塞米松治疗组。卵清蛋白致敏并激发后采用间接免疫荧光法检测气道和肺组织中CARM1和NF-B(P65)的表达,探讨其在哮喘中可能的作用机制。结果:CARM1和NF-κB(P65)在对照组、哮喘组及地塞米松治疗组均有阳性表达,主要在支气管-终末细支气管上皮细胞和肺组织细胞胞核表达。CARM1和NF-κB(P65)在哮喘组表达水平为([123.75±41.55)和(126.92±46.74)],在地塞米松治疗组表达水平为([84.33±27.70)和(85.00±29.22)],均高于对照组的([51.67±8.29)和(52.75±9.07)个/400倍视野],地塞米松治疗组表达较哮喘组低。结论:CARM1和NF-B(P65)在哮喘豚鼠气道上皮及肺组织细胞胞核高表达,提示CARM1可能通过增强募集NF-B到相关位点激活NF-B信号转导通路并启动了多种前炎性基因和免疫调节基因的转录激活、诱发哮喘炎症反应。地塞米松可下调CARM1和NF-κB的表达而抑制哮喘炎症反应。Objective： To investigate the expression of coactivator-associated arginine methyltransferase 1（CARM1）and nuclear factor kappaB（NF-κB（P65）） in airway and lungs of guinea pigs in asthma model and the interference effect of dexamethasone.Methods： Thirty six white male guinea pigs were randomly Divided into control group,asthma group and dexamethasone administration group.After OVA-sensitization and OVA challenge indirect immunofluorescence were used to examine CARM1and NF-κB（P65）expression in airway and lungs to explore its potential mechanism in asthma.Results： The positive expression of CARM1and NF-κB（P65）were detected in all groups,they were mainly expressed on the nucleus of bronchial-terminal bronchiolar epithelium and lungs.The expression of CARM1 and NF-κB（P65） significantly increased in asthma group[（123.75±41.55）and（126.92±46.74）]and dexamethasone group [（84.33±27.70）and（85.00±29.22）] compare with the control group[（51.67±8.29）and（52.75±9.07）/400 field].The expression of dexamethasone group decreased compare with the asthma group.Conclusions： CARM1 and NF-κB（P65） highly express in the airway epithelium nucleus and lung cell nucleus of asthmatic guinea pigs.These results suggest that CARM1 may activate NF-κB signal transduction pathway by enhancing NF-κB recruitment to cognate sites and initating transcriptional activation of a variety of proinflammatory and immunoregulation gene,therefore induce asthma inflammatory reaction.Dexamethasone downregulate the expression of CARM1and NF-κB and inhibit asthma inflammatory reaction.

关 键 词：哮喘 精氨酸甲基转移酶1 核因子-ΚB 

分 类 号：R562.2[医药卫生—呼吸系统]