中文摘要：

龙血竭是一种传统的镇痛抗炎药物,为进一步明确龙血竭镇痛作用的主要部位,本文研究了来自剑叶龙血树的龙血竭总黄酮（Total Flavonoids of Dragon’s blood,TFD）的镇痛作用及其机制。通过在体实验评价TFD的镇痛效果及其急性毒性,利用全细胞膜片钳技术研究其对大鼠背根神经节神经元上TRPV1和电压门控性钠离子通道的作用。实验结果显示2-20 mg/kg剂量的龙血竭总黄酮对福尔马林模型第Ⅱ相疼痛有显著抑制效果;0.02-2 mg每只小鼠剂量的TFD可以显著降低辣椒素引起的舔脚时间。上下法急性毒性实验表明TFD对小鼠的LD50大于5 g/kg。TFD对1μmol/L辣椒素所激发的TRPV1电流的最大抑制率为（50.6±2.2）%,半数抑制浓度为（10.6±0.8）μg/m L。TFD浓度依赖性地抑制电压门控性TTX-s和TTX-r型钠离子通道电流,其对TTX-s和TTX-r型钠通道的半数抑制浓度分别是（19.8±3.0）μg/m L和（36.3±4.6）μg/m L。TFD可升高TTX-s和TTX-r型钠通道的半激活电压,并降低它们的半失活电压。TFD具有较好的镇痛作用并且无明显急性毒性,它的镇痛效应的机制之一是通过在痛觉传输通路上同时对电压门控性钠通道和TRPV1受体进行调制而起作用。

英文摘要：

Dragon＇s blood is one of the renowned traditional medicines used for treatment of various diseases. This study was aimed to evaluate the analgesic effect of total flavonoids of Dragon＇s blood（TFD） from Dracaena cochinchinensis（Lour.） S. C. Chen in animal models and its effects on TRPV1 receptor and voltage-gated sodium channels in acutely dissociated rat DRG neurons by using whole-cell patch clamp technique. The TFD（2-20 mg/kg, i.p.） showed significant analgesic activity in the phase Ⅱ of formalin test and it significantly reduced capsaicin-induced licking time in all doses tested in mice. The LD50 of TDF in mice is greater than 5 g/kg by up-and-down procedure. TFD inhibited 1 μM capsaicin activated current in DRG neurones, and its maximal inhibition efficiency was（50.6±2.2）%, half-maximal inhibitory concentration was（10.6±0.8） μg/m L. TFD also inhibited both TTX-s and TTX-r sodium currents in dose-dependent manner, and the half-maximal inhibitory concentrations of TFD for TTX-s and TTX-r sodium channels were（19.8±3.0） μg/m L and（36.3±4.6） μg/m L, respectively. TFD could increase the half-maximal activation voltage and reduce the half-maximal inactivation voltage for both TTX-s and TTX-r sodium channels. These results indicated that the TFD have significant analgesic activity and did not show significant acute toxicity. One mechanism of analgesic effect of TFD is that it modulates both TRPV1 receptor and voltage-gated sodium channels simultaneously in pain transmission pathways.