摘要
目的:探讨共激活因子相关的精氨酸甲基转移酶1和核因子-κB在豚鼠支气管哮喘模型气道和肺组织的表达变化。方法:24只白色雄性豚鼠随机分为:①正常对照组;②哮喘组。卵清蛋白致敏并激发后采用间接免疫荧光法检测气道及肺组织精氨酸甲基转移酶1和核因子NF-κB(P65)的表达水平,探讨其在哮喘中可能的作用机制。结果:CARM1和NF-κB(P65)在对照组和哮喘组均有阳性表达,主要在支气管—终末细支气管上皮细胞和肺组织成纤维细胞胞核表达。正常对照组和哮喘组CARM1和NF-κB(P65)的表达差异均有统计学意义。结论:在哮喘豚鼠气道上皮及肺组织CARM1和NF-κB(P65)在细胞胞核高表达,提示CARM1可能通过增强募集NF-κB到相关位点激活NF-κB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从而诱发哮喘炎症反应。
Objective: To investigate the expression of coactivator-associated arginine methyltransferase 1 and nuclear factor kappaB in airway and lungs of guinea pigs in a OVA (ovalbumin)-asthma model. Methods: Twenty four white male guinea pigs were randomly divided into control group and asthma group. After OVA-sensitization and OVA-challenge indirect immunofluorescence were used for examining CARMland NF-κB (P65) expression in airway and lungs to explore its potential mechanismin asthma. Results: The positive expression of CARM1 and NF-κB (P65)were detected in all groups,they were mainly expressed on the nucleus of bronchial terminal bronchiolar epithelium and lung fibroblasts. The expression of CARM1 and NF-κB(P65 )had statistical significance between asthma group and control group.Conclusion CAR-M1 and NF-κB ( P65 )highly express in the nucleus in the airway epithelium and lungs of asthmatic guinea pigs. These results suggest that CARM1 maybe activate NF-κB signal transduction pathway by enhancing NF-κB recruitment to cognate sites and starting transcriptional activation of a variety of proinflammatory and immunoregulation gene as a result of inducing asthma inflammatory reaction.
出处
《现代生物医学进展》
CAS
2008年第5期820-821,824,F0002,共4页
Progress in Modern Biomedicine