【摘要】 目的观察芍药苷的镇痛作用与大鼠三叉神经节神经元上酸敏感离子通道（ASICs）的关系。方法制备口面部5%甲醛炎性疼痛模型,通过大鼠自发痛行为评估芍药苷的镇痛作用;采用全细胞膜片钳技术,探讨芍药苷对大鼠三叉神经节神经元ASICs介导的H⁺激活电流(I_asic)的调制作用。结果①大部分受检细胞（82.4%）对酸性外液敏感,可记录到具有pH依赖性的内向电流,该电流可被ASICs拮抗剂阿米诺利阻断。②预加芍药苷(10～1000μmol·L^-1)对I_asic有抑制作用,该抑制作用呈可逆性和浓度依赖性,腺苷A1受体特异性拮抗剂DPCPX可阻断芍药苷的抑制作用;③芍药苷使I_asic量效曲线明显下移,最大反应浓度时I_asic减少了（54.89±4.94）%,但pH₅₀值无明显改变。④腹腔注射芍药苷(50 mg·kg^-1)或面部皮下注射阿米洛利（30μg）可明显缩短5%甲醛诱导的第二相洗面持续时间,预先皮下注射DPCPX（10μg）可部分阻断芍药苷镇痛作用。结论芍药苷镇痛效应与其作用于A1受体进而抑制I_asic有关。更多还原

【Abstract】 Objective To investigate whether acid-sensing ion channels（ASICs） in rat trigeminal ganglion（ TG） neurons was involved in the anti-nociceptive effects of paeoniflorin（Pae）. Methods Rat orofacial formalin pain model was used to evaluate the anti-noceciptive effect of Pae.Whole-cell patch clamp technique was used to record proton-gated currents mediated by ASICs(I_asic ) in TG neurons. Results ① The majority of examined neurons（82.4%） were sensitive to acidic extracellular medium.The acidic extracellular medium induced inward current in a pH-dependent manner, and I_asic were blocked by amiloride, an antagonist of the ASICs.② When Pae(10-1000 μmol·L^-1)was pre-applied extracellularly, it reduced I_asic significantly in TG neurons, this inhibitory effect was reversible and dose-dependent, the inhibition of I_asic by Pae could be partially reversed by pre-application of DPCPX（ antagonist of adenosine A1 receptor）.③ The pH-dependent activation curve was shifted downwards by Pae, with a decrease of（54.89±4.94）% in the maximum amplitude of I_asic but with no significant change in the pH₅₀ value.④ Pae( 50 mg·kg^-1,ip) or amiloride（ 30 μg, sc） significantly attenuated the second phase of the face-rubbing response induced by formalin, the antinociceptive effects of Pae were partially reversed by DPCPX（10 μg, sc）. Conclusion These results suggest that the analgesics effect of Pae may be due to the inhibition of ASICs via adenosine A1 receptor in rat primary sensory neurons.更多还原