文章摘要
王永梅,李 婷,胡玉龙,李 菁,陈 亮,李跃华.核因子-κB参与压力负荷性心力衰竭的发病机制研究[J].南京医科大学学报,2007,(8):777~780784
核因子-κB参与压力负荷性心力衰竭的发病机制研究
Nuclear factor-κB is required for pressure overload-induced heart failure
投稿时间:2007-02-04  
DOI:10.7655
中文关键词: 心力衰竭  信号转导  核因子-κB
英文关键词: heart failure  signaling pathway  nuclear factor-κB
基金项目:国家自然科学基金资助项目(30571842)和南京医科大学科技创新基金资助项目(CX2004001)
作者单位
王永梅 南京医科大学病理生理学系,江苏 南京 210029 
李 婷 南京医科大学病理生理学系,江苏 南京 210029 
胡玉龙 南京医科大学病理生理学系,江苏 南京 210029 
李 菁 南京医科大学病理生理学系,江苏 南京 210029 
陈 亮 南京医科大学第一附属医院心胸外科,江苏 南京 210029 
李跃华 南京医科大学病理生理学系,江苏 南京 210029 
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中文摘要:
      目的:研究核因子-κB(NF-κB)在心脏压力负荷增加所诱导的心力衰竭的发病过程中的相关改变?方法:SD大鼠采用主动脉弓部缩窄术,术后12周对大鼠进行心功能分析;采用心肌组织Masson染色评估术后纤维化程度;凝胶迁移率电泳(electrophoretic mobility shift assay,EMSA)方法检测心肌组织中NF-κB结合活性改变;并利用免疫共沉淀方法(immunoprecipitation,IP)对上游信号分子Toll-like receptor4(TLR4) 与 myeloid differentiation primary-response protein 8(MyD88) 的相互结合作用进行分析?结果:SD大鼠术后12周心脏收缩及舒张功能与假手术组相比较均有明显下降, 其心肌组织纤维化程度明显加重? NF-κB在肥大心肌组织中的结合活性与周龄适配的假手术组相比显著增加(P < 0.05), 其上游两个重要的信号分子TLR4/MyD88的相互结合作用增强(P < 0.05)?结论:NF-κB参与了压力负荷增加诱导的心力衰竭的发病过程的调控?
英文摘要:
      Objective:To study nuclear factor-κB(NF-κB) activation in heart failure due to chronic pressure-overload. Methods: SD rats were performed by transverse aortic banding for 12 weeks. After that hemodynamic parameters and cardiac fibrosis were measured;NF-κB binding activity was analyzed by electrophoretic mobility shift assay(EMSA);Immunoprecipitation(IP) was performed to analysis Toll-like receptor 4(TLR4) and myeloid differentiation primary-response protein 8(MyD88) association. Results:Both systolic and diastolic function were significantly reduced compared with sham operated group(P < 0.05), and cardiac fibrosis enhanced predominantly. NF-κB binding activity in hypertrophic heart tissue was higher than that of sham operated group(P < 0.05) as well as TLR4/MyD88 association(P < 0.05). Conclusion:NF-κB was required for chronic pressure overload-induced heart failure.
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