周围神经损伤是以局部或四肢远端疼痛、麻木为主要症状的临床常见病症，运用推拿治疗，效果满意。但临床对其起效的机制阐述，尚停留在经典理论层面，如“通经止痛”等，经典与机理之间尚未找到契合点。我们前期研究发现，推拿能够通过提高肌肉、神经、脊髓等组织中神经营养因子的表达，促进损伤神经的修复。近期研究亦表明，轴浆运输的中断阻碍了损伤神经的修复；促炎性因子表达的升高、致痛物质的产生，是导致炎性痛与神经性病理痛发生的关键。因此，本次研究拟采用HRP逆行示踪、神经髓鞘染色、神经电生理检测、酶联免疫、免疫组化、Western-blot等技术，着眼于CCI（坐骨神经慢性压迫损伤摸型）大鼠体内微环境（损伤点、脊髓、血清）中关键指标马达蛋白（dynein、kinesin、dynactin）、促炎性因子（IL-1、IL-6、TNF-α、PGE2）表达的变化，结合行为学、形态学改变，揭示推拿“通经止痛”的科学内涵。

Peripheral nerve injury is a common clinical disease, the main symptom being local or distal limb pain or numbness; the treatment of this disease with tuina yields satisfactory results. But the explanation of the mechanism behind this clinical effectiveness stops at the classical theory level, such as "Tongjing Zhitong", etc, mechanism and classical theory have yet to find a meeting point. Our initial research revealed that tuina can increase the expression of neurotrophic factors in muscle, nerve, spinal cord and other tissues, and thereby accelerate neural repair. Recent research also suggests that, interrupted axoplasmic transport hinders neural repair; increased expression of inflammatory cytokines and pain-producing substances are key causes of inflammatory pain and neuropathic pain. Therefore, this study adopts various techniques including HRP retrograde tracing, myelin staining, electrocardiography, ELISA, immunohistochemistry, Western-blot, etc, and focuses on the key indicator motor proteins (dynein, kinesin, dynactin), expression changes in inflammatory cytokines (IL-1, IL-6, TNF- α, PGE2), and combined ethological and morphological changes of the internal micro-environment (site of injury, spinal cord, serum) of CCI (chronic constriction injury of the sciatic nerve) model rats, in order to reveal the underlying scientific basis for tuina’s effect of "moving the meridians to stop pain”.