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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 changes of coactivator-associated arginine methyltransferase1 (CARM1) and nuclear factor-B (NF-B) in airway and lung tissue in guinea pig bronchial asthma model, The effect of dexamethasone intervention. Methods: Thirty-six white male guinea pigs were randomly divided into normal control group, asthma group and dexamethasone treatment group. Ovalbumin sensitized and challenged by indirect immunofluorescence detection of airway and lung tissue CARM1 and NF-B (P65) expression, explore its possible role in the mechanism of asthma. Results: The expressions of CARM1 and NF-κB (P65) in the control group, the asthma group and the dexamethasone group were both positive and mainly expressed in the nuclei of bronchial-terminal bronchial epithelial cells and lung tissues. The expression levels of CARM1 and NF-κB (P65) in asthmatic group were (123.75 ± 41.55) and (126.92 ± 46.74), respectively, and those in dexamethasone group were (84.33 ± 27.70) and (85.00 ± 29.22) , Which were higher than those in the control group ([51.67 ± 8.29] and (52.75 ± 9.07) / 400 times). The dexamethasone treatment group had lower expression than the asthma group. CONCLUSIONS: CARM1 and NF-B (P65) are highly expressed in the nucleus of airway epithelium and lung tissue of asthmatic guinea pigs, suggesting that CARM1 may activate NF-B signal transduction pathway and enhance the expression of NF- Transcriptional activation of pro-inflammatory and immunomodulatory genes induces an inflammatory response in the asthma. Dexamethasone can down-regulate the expression of CARM1 and NF-κB to inhibit the inflammatory response of asthma.