TLR-3在骨骼肌萎缩中的作用

The role of TLR-3 in skeletal muscle atrophy

[目的]禁食、慢性疾病等会导致肌肉萎缩的发生,临床表现为肌肉质量下降、肌纤维直径变小、肌肉张力以及抗疲劳能力下降等。有研究显示,小鼠成肌细胞C2C12中7种Toll样受体(Toll-like receptors,TLRs)均表达,为了进一步研究TLR家族中TLR-3在肌萎缩中的作用机制,探讨治疗肌萎缩的新方法。[方法]以小鼠C2C12细胞为实验材料,地塞米松处理构建肌肉萎缩模型,转染si TLR-3后通过免疫荧光、q PCR和Western Blot方法检测对肌细胞萎缩模型的改善情况。[结果]发现干涉TLR-3能明显改善细胞萎缩模型的表型,并使肌萎缩标志性基因MuRF和MAFbx在mRNA水平和蛋白水平均明显下调。[结论]以上结果说明干涉TLR-3改善了成肌细胞肌萎缩症状,该研究为探明Toll样受体家族在肌萎缩中的作用机制,及肌肉疾病的防治奠定基础。

[Objective]Fasting,chronic diseases can lead to muscle atrophy,clinical manifestations of decreased muscle mass,muscle fiber diameter,muscle tension and anti-fatigue ability decline.Studies had shown that seven Toll-like receptors(TLRs)were expressed in the mouse myoblasts C2 C12 cell line and interference TLR-2 or TLR-4 could improve muscular atrophy.[Method]To study the function mechanism of TLR family protein TLR-3 in muscular atrophy,C2 C12 cell line was used as the experimental material to build muscular atrophy model by dexamethasone treatment and transfection with si TLR-3,then through immunofluorescence,q PCR,Western Blot and other methods to detect the improvement of muscle cell atrophy.[Result]We found that interfered the TLR-3 gene can significantly improve muscle atrophy and down regulate muscular atrophy markers MuRF and MAFbx.[Conclusion]We confirmed that TLR3 play an important role in the regulating of occurrence of muscular atrophy,lay the foundation of exploring the mechanis of Toll-like receptor family in muscular atrophy,and it’s helpful for prevention and treatment of muscle disease.