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作 者:张路路 洪江茹 苏亦睿 刘文涛[2] 张广钦[1] ZHANG Lulu;HONG Jiangru;SU Yirui;LIU Wentao;ZHANG Guangqin(Department of Clinical Pharmacy,China Pharmaceutical University,Nanjing 211198,China;Jiangsu Provincial t(ey Laboratory for Neurodegenerative Diseases,Nanjing Medical University,Nanjing 211166,China)
机构地区:[1]中国药科大学临床药学教研室,江苏南京211198 [2]南京医科大学江苏省神经退行性疾病重点实验室,江苏南京211166
出 处:《药学研究》2018年第11期625-629,共5页Journal of Pharmaceutical Research
基 金:国家自然科学基金资助项目(No.81471142)
摘 要:目的本文通过观察芍药苷(paeoniflorin,Pae)对小鼠背根神经节(dorsal root ganglion,DRG)细胞电压门控河豚毒素敏感型(TTX-S)钠电流的影响,探讨芍药苷的镇痛机制。方法应用全细胞膜片钳技术在急性分离背根神经节细胞上记录河豚毒素敏感型钠电流。结果芍药苷浓度依赖地抑制河豚毒素敏感型钠电流,其半抑制浓度(IC50)为1224.1μmol·L^(-1)。芍药苷1 mmol·L^(-1)使河豚毒素敏感型钠通道的失活曲线向超极化方向转移约7.1m V,并且延迟失活后通道的恢复,但对激活曲线没有影响。结论芍药苷可能通过抑制河豚毒素敏感型钠通道,改变钠通道的动力学特征,从而发挥其镇痛作用。Objective To explore the analgesic mechanism of Pae by investigating the effects of Pae on voltage-gated tetrodotoxin sensitive (TTX-S) sodium current in mouse dorsal root ganglion (DRG) neurons. Methods The whole-cell patch clamp technique was used to investigate TTX-S sodium current in freshly isolated DRG neurons. Results Pae had a concentration-dependent inhibition on TTX-S sodium current with a half-inhibitory concentration (IC 50 ) of 1 224.1 μmol·L -1 .1 mmol·L -1 of Pae shifted the inactivation curve of TTX-S sodium current to the direction of hyperpolarization by about 7.1 mV and delayed the recovery of the TTX-S sodium current after inactivation,but had no effect on the activation curve. Conclusion Pae significantly inhibited TTX-S sodium channels and changed the kinetic characteristics of the channels.These effects of Pae may be related to its analgesia.
关 键 词:芍药苷 河豚毒素敏感型钠通道 全细胞膜片钳技术 背根神经节
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