Article Summary
杨菲 张统一 白录军 徐春华 方相春.人参皂甙Rd通过调节SNI大鼠背根神经节钠、钾电流抑制痛敏[J].现代生物医学进展英文版,2014,14(12):2214-2218.
人参皂甙Rd通过调节SNI大鼠背根神经节钠、钾电流抑制痛敏
Ginsenoside Rd Inhibits Mechanical Pain Hypersensitivity ThroughModulating the Voltage-gated Sodium and Potassium Current in DRGNeurons in Rats of Spared Sciatic Nerve Injury
  
DOI:
中文关键词: 人参皂甙Rd  机械性痛敏  钠电流  钾电流
英文关键词: Ginsenoside Rd  Mechanical pain hypersensitivity  Sodiumcurrent  Potassiumcurrent
基金项目:国家自然科学基金项目(81070899)
Author NameAffiliation
YANG Fei, ZHANG Tong-yi, BAI LU-jun, XU Chun-hua, FANG Xiang-chun 第四军医大学唐都医院疼痛生物医学研究所
兰州军区临潼疗养院第二疗养区
第四军医大学人体解剖与组织胚胎学教研室暨梁銶琚脑研究中心 
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中文摘要:
      目的:观察人参皂甙Rd(ginsenoside Rd)对大鼠坐骨神经分支选择性损伤(spared sciatic nerve injury, SNI)引起的痛敏的影 响及其作用机制。方法:坐骨神经分支选择性损伤术后7 天,观察腹腔注射不同浓度人参皂甙Rd 后大鼠后足的机械性缩足反应 阈值(paw withdrawl mechanical threshold, PWMT)的变化;在术后7 天,急性分离并取出大鼠腰4 和腰5 段背根节,对整节DRG 上的中小型神经元运用全细胞膜片钳技术进行记录。结果:坐骨神经分支选择性损伤术后7 天,大鼠出现明显的机械性痛敏,腹 腔注射5 mg/ml和10 mg/ml的人参皂甙Rd 能剂量依赖性的翻转大鼠机械性痛敏;坐骨神经分支选择性损伤能明显地增大SNI 大鼠DRG中小型神经元上的钠电流以及减小电压依赖性钾电流,而100 uM 人参皂甙Rd 能有效翻转该钠、钾电流的变化。结 论:人参皂甙Rd 能有效地改善坐骨神经分支选择性损伤引起的机械性痛敏,其机制可能与人参皂甙Rd 明显地调节SNI 大鼠 DRG中小型神经元上的电压依赖性钠、钾电流有关。
英文摘要:
      Objective:To evaluate the effect of ginsenoside Rd on the mechanical pain hypersensitivity in rats with spared sciatic nerve injury and probe the potential underlying mechanism.Methods:7 day post SNI, the paw withdrawl mechanical threshold was measured before and after intraperitoneal administration of ginsenoside Rd in rats with mechanical pain hypersentivity; the L4 and L5 DRG were isolated acutely, and whole-cell recording patch clamp were performed on small- and medium-sized DRG neurons.Results:Ginsenoside Rd could dose-dependently reduce mechanical pain hypersentivity induced by spared sciatic nerve injury; electrophysiological recordings showed that ginsenoside Rd could decrease the voltage-gated sodium current and increase the voltage-gated potassium current in small- and medium-sized DRG neurons in rats with SNI.Conclusion:Ginsenoside Rd could reversed the mechanical pain hypersensitivity in rats with SNI, and the potential mechanism might relate to the modulating effect of ginsenoside Rd on the voltage-gated sodiumcurrent and the voltage-gated potassiumcurrent.
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