中文摘要：

[目的]探讨神经痛维持期脊髓背角辣椒素受体（transient receptor potential vanilloid type1,TRPV1）的活化形式及低频电针的干预作用。[方法]将SD大鼠随机分为正常组（normal组）、假手术组（sham SNI组）、模型组（SNI组）和电针组（2Hz EA组）,每组8只。建立大鼠坐骨神经分支选择性损伤（spared nerve injury,SNI）模型,取术侧足三里、昆仑穴进行2Hz电针干预,每日1次,连续14天,检测大鼠术侧后足缩腿阈（paw withdrawal threshold,PWT）,观察大鼠痛觉超敏反应。运用免疫印迹法检测术侧脊髓背角TRPV1、p-TRPV1及蛋白激酶C（protein kinase C,PKC）水平,用免疫荧光法检测术侧脊髓背角TRPV1及PKC阳性细胞表达情况。[结果]SNI模型大鼠维持期出现痛觉过敏,PWT下降（P〈0.01）,术侧脊髓背角TRPV1水平、PKC水平均升高（P〈0.01）,p-TRPV1水平无显著变化（P〉0.05）,sham SNI组大鼠PWT无明显变化。低频电针提高SNI模型大鼠的PWT（P〈0.01）,降低脊髓背角TRPV1与PKC水平（P〈0.01）。[结论]神经痛维持期脊髓背角TRPV1活化以表达上调为主。低频电针能改善维持期神经痛,其机制可能与其有效下调PKC介导的TRPV1信号通路有关。

英文摘要：

[Objective] To investigate the activation modes of spinal cord dorsal horn（ SCDH） transient receptor potential vanilloid type 1（ TRPV1）at maintenance period of neuropathic pain and the effect of electroacupuncture（EA） with low frequency. [Methods] SD rats were randomly divided into Normal, Sham spared nerve injury（SNI）, SNI and SNI ＋ EA groups, 8 animals per group. Rat neuropathic pain model was established with SNI. 2Hz EA was administered at ipsilateral points Zusanli（ST36） and Kunlun（BL60） once every day for consecutive 14 days. Paw withdrawal threshold（PWT） was tested to determine mechanical allodynia. The levels of TRPV1, p-TRPV1 and protein kinase C（PKC） in ipsilateral SCDH were tested by western blotting.The positive cells of TRPV1 and PKC expressions were measured by immunofluorescence. [Results] Rats in SNI group developed spontaneous pain at maintenance period of neuropathic pain and showed a significant reduction in PWT（P〈0.01）. The ipsilateral SCDH TRPV1 level and PKC level both increased（P〈0.01）, while p-TRPV1 level had no significant changes（P〈0.05）. Rats in sham SNI group had no obvious changes. 2Hz EA up-regulated SNI rats PWT（P〈0.01）, reduced ipsilateral SCDH TRPV1 level and PKC level. [Conclusion] SCDH TRPV1 activation is mainly through its enhancement of expression. Electroacupuncture with low frequency could alleviate neuropathic pain during the maintenance period, which may be related to the down-regulation of TRPV1 signal transduction pathway which mediated by PKC.