miR-206在腭帆张肌放射性损伤中的表达及机制研究

分泌性中耳炎是鼻咽癌放疗后发生率较高的并发症。前期研究发现腭帆张肌（TVP）的放疗损伤导致了咽鼓管的主动开放功能障碍引起分泌性中耳炎，主要表现为肌源性的损伤，但机制仍未明确。随着骨骼肌特异性miRNAs成为研究肌肉损伤的热点，其中miR-206及其调控的靶基因HDAC4及SRSF9在骨骼肌损伤修复中的作用尤为重要。由此，我们提出假设：在TVP放射性损伤中，miR-206通过调控SRSF9、HDAC4引起TVP的修复、再生障碍，导致其萎缩及纤维化。本项目拟应用树鼩建立放疗后分泌性中耳炎的动物模型并采用组织块反复贴壁法分离培养TVP成肌细胞，通过慢病毒介导的转染技术，检测照射后TVP中SOD、MDA以及miR-206、HDAC4、SRSF9的表达水平，深入探讨TVP放射性损伤的分子机制。对于发展精准的TVP放疗后损伤的治疗方法以及提高放疗后分泌性中耳炎的治愈率具有重要意义。

Secretory otitis media is a high incidence after radiotherapy of nasopharyngeal carcinoma (NPC ) complications . Prophase studies found tensor veli palatine (TVP ) the radiation damage to open led to the initiative in the eustachian tube dysfunction caused by secretory otitis media , main show is muscle damage source sex , but the mechanism is still not clear . As the skeletal muscle specific miRNAs are becoming a hot spot of research on muscle damage , including miR-206 and its regulation of target genes HDAC4 and SRSF9 role in skeletal muscle damage is particularly important . Thus , we hypothesized that in TVP radioactive damage , miR-206 through regulating SRSF9 , HDAC4 cause disorder of TVP repair and regeneration , causes the atrophy and fibrosis . Tree shrews applied to this project to establish animal model of secretory otitis media after radiotherapy and uses the tissue block repeatedly adherent cultivation method in TVP myoblast , by Lentivirus mediated transfection technique ,testing TVP after irradiation of SOD , MDA and miR-206 , HDAC4 ,SRSF9 expression level , and discusses the molecular mechanisms of TVP radioactive damage . For the development of precision TVP damage after radiotherapy treatment and improve the cure rate of secretory otitis media after radiotherapy is of great significance .