论文部分内容阅读
目的:探讨脱氧鬼臼毒素(DOP)对外周神经系统的毒性作用机制。方法:采用全细胞膜片钳技术研究DOP对急性分离大鼠背根(DRG)神经元电压依赖性钾通道的作用,从离子通道水平探讨其神经毒性作用机制。结果:10、20、40、80μmol/L的DOP对全钾电流(IK)和延迟整流钾电流(IKDR)均有影响,且能以浓度依赖方式、部分可逆地阻断电压依赖性钾电流,使电流电压曲线向去极化方向移动。同时,DOP对IKDR的抑制率[(43.22±6.85)%]明显高于IK[(27.55±4.65)%]。结论:DOP对钾离子电流的影响可能是鬼臼毒素类化合物引起外周神经病变的机制之一。
Objective: To investigate the toxic mechanism of deoxypodophyllotoxin (DOP) on the peripheral nervous system. Methods: Whole-cell patch-clamp technique was used to study the effect of DOP on voltage-dependent potassium channel in acutely isolated rat dorsal root ganglion (DRG) neurons. The mechanism of neurotoxicity was explored from ion channel level. Results: DOP at 10, 20, 40 and 80 μmol / L had effects on both total potassium current (IK) and delayed rectifier potassium current (IKDR), and partially and reversibly blocked voltage-dependent potassium current in a concentration-dependent manner So that the current voltage curve to the direction of depolarization. At the same time, the inhibitory rate of DOP to IKDR [(43.22 ± 6.85)%] was significantly higher than that of IK [(27.55 ± 4.65)%]. Conclusion: The effect of DOP on potassium current may be one of the mechanisms of podophyllotoxin-induced peripheral neuropathy.