基于NDRG2/GLT-1介导星形胶质细胞调控突触可塑性探讨推拿干预腰椎间盘突出症的镇痛机制

腰椎间盘突出症（LDH）是引起腰腿痛的常见病。推拿对LDH具有良好的镇痛效果，但其机制尚未明确。研究表明，脊髓背角星形胶质细胞中NDRG2调控GLT-1，减少突触间隙谷氨酸及其受体NMDA的含量，影响突触可塑性，是改善LDH疼痛的重要原因。我们前期研究发现，推拿对LDH镇痛作用明显，且能降低LDH大鼠脊髓背角谷氨酸及NMDAR含量，调节突触可塑性。为此，我们推测：推拿可能通过减轻突触周围星形胶质细胞的活化，抑制星形胶质细胞中NDRG2，上调GLT-1，降低突触间隙谷氨酸浓度及其受体NMDA表达，调节突触可塑性，从而对LDH起到镇痛作用。本项目拟采用疼痛行为学、细胞生物学、电生理学等多学科技术方法，观察推拿对LDH大鼠星形胶质细胞中NDRG2/GLT-1通路调控谷氨酸和NMDAR的作用，以及对突触传递效能的影响，探讨推拿对LDH的具体镇痛机制，为运用推拿改善LDH疼痛提供理论依据和实验基础。

Lumbar disc herniation (LDH) is a clinically common condition causing low back and leg pain. Massage has a good analgesic effect on LDH, but its mechanism remains unclear. Studies have shown that NDRG2 in spinal dorsal horn astrocytes regulates GLT-1, reduces the content of glutamate and its receptor NMDA in synaptic space, and affects synaptic plasticity, which is an important reason for the improvement of LDH pain. Our previous study found that massage has obvious analgesic effect on LDH, and can reduce glutamate and NMDAR contents and regulate synaptic plasticity, in the spinal dorsal horn of LDH rats. Therefore, we hypothesized that massage may play an analgesic role on LDH by reducing the activation of perisynaptic astrocytes, inhibiting NDRG2 in astrocytes, upregulating GLT-1, reducing the concentration of glutamate in synaptic space and regulating the expression of its receptor NMDA, and regulating synaptic plasticity. This project intends to adopt pain behavior, cell biology and electrophysiology multidisciplinary technology and methods, to observe the massage of LDH rat astrocyte glutamate NDRG2/GLT-1 channel regulation and the role of the NMDA receptor, and the influence on synaptic transmission efficiency, explore the massage specific analgesic mechanism of LDH, so as to provide theoretical basis and experimental basis for using massage to improve LDH pain.