基于cAMP-PKA通路研究电针调控终板软骨细胞AQP1、3在防治腰椎间盘退变中的作用及机制

Lumbar intervertebral disc degenerative diseases are clinical multiple and easy to relapse. So researches on prevention and treatment of lumbar disc degeneration have been the focus of attention by the international research field. How to control degenerative disc initiating factor and promote the repairment of degenerative disc tissue has very important practical significance. Our preliminary studies showed that electroacupuncture(EA) displayed good therapeutic effects on lumbar degenerative disc diseases and could retard disc degeneration. To further clarify the regulatory mechanism of EA for disc degeneration, this project will confirm the evidence of EA on AQP1、3 expression in endplate chondrocytes of the rabbit model of degenerative lumbar disc firstly, testify the protective effect of EA on initiating factors of lumbar disc degeneration, then, to study the active mechanism of cAMP-PKA pathway on regulation of AQP1、3 expression of EA through establishment of lumbar disc degeneration model, to enhance water-based nutrient supply by cartilage endplate channel, applying the means of diffusion tensor imaging, molecular biology and laser scanning confocal microscope, integrating a variety of research and the basis of our own work. This study will help to reveal the mechanisms of molecular biology and signal transduction of EA, and provide scientific experimental basis for the clinical practice of EA on prevention and treatment for lumbar degenerative disc disease.

腰椎间盘退变性疾病临床多发，且易复发，因此，对腰椎间盘退变的防治研究，一直是国际相关研究领域的焦点。如何控制腰椎间盘退变的始动因素，促进退变椎间盘组织的修复，具有十分重要的现实意义。前期研究表明，电针对腰椎间盘退变性疾病具有良好的治疗作用且能延缓椎间盘退变，为进一步明确电针对椎间盘退变的调控机制，本项目综合各种研究和自身工作基础，通过建立腰椎间盘退变模型，应用DTI、分子生物学及激光共聚焦等技术手段，首先证实电针对模型兔退变腰椎间盘终板软骨细胞AQP1、3表达的影响证据，明确电针对腰椎间盘退变始动因素的保护作用，并进一步研究cAMP-PKA信号通路在电针调控AQP1、3表达、增加软骨终板途径以水为主的营养供应、延缓椎间盘退变中的作用及机制。本研究将有助于揭示电针防治腰椎间盘退变的分子生物学及其信号转导机制，为临床运用电针防治腰椎间盘退变性疾病提供科学实验依据。

腰椎间盘退变性疾病临床多发，且易复发，因此，对腰椎间盘退变的防治研究，一直是国际相关研究领域的焦点。如何控制腰椎间盘退变的始动因素，促进退变椎间盘组织的修复，具有十分重要的现实意义。前期研究表明，电针对腰椎间盘退变性疾病具有良好的治疗作用且能延缓椎间盘退变，为进一步明确电针对椎间盘退变的调控机制，本项目综合各种研究和自身工作基础，通过建立腰椎间盘退变模型，应用DTI、分子生物学及激光共聚焦等技术手段，首先证实电针对模型兔退变腰椎间盘终板软骨细胞AQP1、3表达的影响 证据，明确电针对腰椎间盘退变始动因素的保护作用，并进一步研究cAMP-PKA信号通路在 电针调控AQP1、3表达、增加软骨终板途径以水为主的营养供应、延缓椎间盘退变中的作用及机制。本研究将有助于揭示电针防治腰椎间盘退变的分子生物学及其信号转导机制，为临床运用电针防治腰椎间盘退变性疾病提供科学实验依据。