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异丙肾上腺素防治失神经骨骼肌萎缩机制研究

异丙肾上腺素防治失神经骨骼肌萎缩机制研究
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摘要 目的:研究异丙肾上腺素对失神经骨骼肌萎缩中NF-κB、MuRF1表达变化的影响,探讨其防治失神经骨骼肌萎缩的机制。方法:选用wista大鼠54只,制作成标准右侧坐骨神经离断、腓肠肌失神经支配模型,随机分为对照组和药物组,应用RT-PCR和Western Bloting检测不同时段的NF-κB、MuRF1mRNA和蛋白质表达水平,联合肌湿重分析其相关性。结果:失神经支配后腓肠肌NF-κB、MuRF1mRNA和蛋白质表达持续增加(P<0.05)。药物组肌湿重和肌细胞横截面积比对照组同时间点明显增加(P<0.05),NF-κB、MuRF1mRNA和蛋白质表达则明显降低(P<0.05)。结论:异丙肾上腺素可以通过抑制NF-κB/MuRF1途径有效防治失神经骨骼肌萎缩。 Objective: To investigate the change of NF - κB and muscle Ring Finger - 1 ( MuRF1 ) on denervation muscle atrophy intervated with isoprel. Methods:Levels of NF - κB and MuRF1 mRNA and protein in gastrocnemins muscle at different time after denervation were detected by RT - PCR and western Blotting. The ratio of muscle wet weight was analyzed for comparison. Result: The level of mRNA and protein of NF - κB and MuRF1 increased correpondingly at different time after denervation ( P 〈 0.05 ) but The group with isoprel decreased at the same time. Conclusion:the change of mRNA and protein presented consistency at different time, and MuRF1 is actively correlated to with increase of levels of NF- κB, indicating that NF - κB/MuRF1 pathway plays an importance role in denervation atrophy of the gastrocnemius,and isoprel is possible to delay denervation muscle atrophy by inhibite the pathway of NF - κB/MuRF1.
出处 《中国社区医师(医学专业)》 2010年第10期8-9,共2页
关键词 失神经骨骼肌萎缩 核因子NF—κB 泛素-蛋白酶体途径肌肉环指因子-1 Denerbated skeletal muscule atrophy Nuclear factor - κB Ubiquitin - proteasomes pathway Muscule ring finger - 1 ( MuRF1 )
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  • 1Agrawal S,Thakur P,Katoch SS,Beta adrenoceptor agonists,clenbuterol,and isoproterenol retard denervation atrophy in rat gastrocnemius muscle:use of 3-methylhistidine as a marker of myofibrillar degeneration.Jpn J Physiol,2003,53:229-237.
  • 2Ishii K,Sowa K,Zhai WG,et al.Effects of a-isoproterenol on denervation atrophy in orbicularis oculi muscle fibers.Histol Histopathol,1998,13:1015-1018.
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