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目的研究去神经致肌萎缩和纤维类型转化的分子机制,探讨TβRII-SMAD信号通路在此过程中的相关性。方法取10只C57BL/6小鼠,右后肢坐骨神经离断,左后肢假手术对照。Real Time PCR(RT-PCR)检测术后14 d比目鱼肌和跖肌萎缩基因MAFbx,MuRF-1,及PGC-1α,MHCIIb,TβRII的表达变化。结果去坐骨神经后萎缩基因MAFbx,MuRF-1及MHCIIb在比目鱼肌和跖肌明显上调;PGC-1α,TβRII的表达在比目鱼肌和跖肌呈现差异性变化。结论 MAFbx,MuRF-1和PGC-1α在肌萎缩过程中发挥重要作用,TβRII可能参与了对肌萎缩的调节。
Objective To study the molecular mechanism of demyelination and fibro type denervation and to explore the correlation of TβRII-SMAD signaling pathway in this process. Methods Ten C57BL / 6 mice were sacrificed, and the right hind limb sciatic nerve was severed and left hindlimb sham operated. Real-time PCR (RT-PCR) was used to detect the expression of MAFbx, MuRF-1, PGC-1α, MHCIIb and TβRII in soleus muscle and plantar muscle atrophy. Results The sciatic nerve atrophy genes MAFbx, MuRF-1 and MHC IIb were significantly upregulated in the soleus and plantar muscles. The expression of PGC-1α and TβRII in the soleus and plantaris muscles varied significantly. Conclusion MAFbx, MuRF-1 and PGC-1α play an important role in the process of muscle atrophy. TβRII may be involved in the regulation of muscle atrophy.