铍针治疗皮神经卡压综合征的临床疗效明确，但是目前铍针对中枢敏化的干预机制仍不详，而中枢敏化是神经病理痛的重要机制之一。MAPK信号转导通路是中枢敏化的关键，但在皮神经卡压综合征急性及慢性疼痛的发生、维持阶段参与中枢敏化的途径尚未明确。本项目拟建立皮神经卡压综合征大鼠模型，系统观察铍针对大鼠腰段脊髓背角ERK1/2磷酸化水平、NK-1及 COX-2 表达（ERK 转导通路）的影响，对p38MAPK、以及VR1 和COX-2 表达（p38MAPK转导通路）的影响，和对JNK1/2、c-Jun 磷酸化水平和AP-1 的DNA 结合活性，以及COX-2表达（JNK 转导通路）的影响，探索铍针治疗皮神经卡压综合征时对MAPK信号通路的干预，揭示铍针治疗皮神经卡压综合征的新原理。并且从细胞转导通路角度、局部软组织力学、组织学、痛行为测定角度探索铍针活血通络的原理。

The clinical curative effect of Pi needle treatment of cutaneous nerve entrapment syndrome is clear, but the intervention mechanism of the Pi needle in central sensitization is still unknown, but the central sensitizationis an important mechanism of neuropathic pain. MAPK signal transduction pathway is a key central sensitization, but in the cutaneous nerve of acute and chronic pain pressure syndrome occurs, the way of keeping the stage incentral sensitization is not clear. This project aims to establish the model of rat skin nerve compression syndrome, Pi needle in rat lumbar spinal dorsal horn, the phosphorylation level of ERK1/2, NK-1 and COX-2 to observe the expression system (ERK pathway) effect on p38 α, MAPK, and VR1 and COX-2 expression (p38MAPK pathway) influence, and on JNK1/2, the level of c-Jun phosphorylation and AP-1 binding activity of DNA, and the expression of COX-2 (JNK pathway) effect, exploration of Pi needle treatment of cutaneous nerve card intervention on MAPK signaling compression syndrome, reveal new principle of Pi needle treatment of cutaneous nerve entrapment syndrome. We shall explore the principle of Pi needle treatment by Huoxue tongluo from cell transduction pathway angle, local soft tissue mechanics, histology, determination of pain behavior perspective.