基于Integrin/FAK信号通路及颈伸肌群力学性能探讨牵伸松调法治疗颈椎病的作用机制

颈椎病是“筋-骨”一体退变的结果，颈伸肌群的病变是退变的前提，椎间盘的退变是基础，软骨终板（CEP）的退变则是椎间盘乃至颈椎退变的起始因素。前期的研究证实，牵伸松调法能调节颈椎病模型兔相关因子的表达，临床应用省时省力，疗效显著。因此，本课题以“重筋顾骨”为治则，“松筋调骨”为治法，提出“手法干预-颈伸肌群超微结构及力学性能改善-外源性平衡能力增强”及“手法干预-CEP超微结构、颈曲及附属关节状态改善-内源性平衡能力提高”双通道起作用的科学假说。拟通过电镜观察实验动物手法干预前后CEP与颈伸肌群肌超微结构变化及p-FAK、NF-κB、MyoD等相关基因的表达，并借助sEMG、PainVision等设备及NPQ、SF-36等量表，从Integrin/FAK信号通路及颈伸肌群力学性能的层面探讨手法治疗颈椎病的机理，多角度、多层次的评估手法治疗颈椎病的临床价值，为推拿治疗颈椎病提供客观科学的依据。

It is confirmed that cervical spondyloysis is the result of degeneration in “jin” and “bone” as a whole, in which the pathological changes of cervical extensors is the premise and cervical disc is the foundation, and CEP is the initial factor of degeneration in disc as well as cervical vertebral body. With the verification of previous study, the manipulation of Extension-Tenolysis-Adjustment(ETA) manipulation can adjust the relative factors expressing in the model rabbits of cervical spondyloysis and is more effective , timesaving and laboursaving in the clinic. Hence, this study take “emphasize jin consider bone” as principle, and “loosen jin adjust bone” as method, put forward the effective binary channels scientific hypothesis of “ETA intervention-- improvement of ultra microstructure and mechanical property of the cervical extensors--enhancement of abilities of exogenous equilibrium” and “ETA intervention--improvement of micro-structure of CEP, cervical abnormal curvature and abnormal state of the accessory structure--strengthening of abilities of endogenous equilibrium”, observing the change of microstructure and gene expression of p-FAK,NF-κB,MyoD of CEP and cervical extensors in experimental animals as well as sEMG,PainVision,scales of NPQ and SF-36 applied in the clinic before and after the ETA intervene, aims to explore the mechanism of ETA on cervical spondylosis based on the signal channel of Integrin/FAK and mechanical property of cervical extensors, to evaluate the clinic value in multiple angles and levels, to provide scientific evidence of Tuina for cervical spondylosis.