蛇床子素对酸诱发髓核致炎大鼠神经节神经元的膜电位改变抑制的作用  

Osthole inhibited the acid-evoked change of membrane potential of rats dorsal root ganglia neuron following application of nucleus pulposus

作　　者：贺秋兰[1] 魏明[1] 李梅娜[1] 徐辉[1] 邹学农[2] 孙来保[1] 

机构地区：[1]中山大学附属第一医院麻醉科,广东广州510080 [2]中山大学骨科研究所,广东广州510700

出　　处：《中国药理学通报》2010年第11期1459-1462,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金广东联合资助重点项目(Nou0732001);广东省自然科学基金面上项目(No8161008901000194);中山大学附属一院与生命科学院联合基金(No162011)

摘　　要：目的研究不同pH酸刺激下髓核致炎大鼠背根神经节(DRG)神经元的膜电位改变,及蛇床子素(Ost)对其的影响。方法移植尾部髓核于左侧腰5DRG建立炎性神经痛大鼠模型,术后3d分离DRG神经元,通过DiBAC4(3)荧光标记,观察不同pH液刺激下胞内荧光强度(膜电位)的动态变化,检测Ost或酸敏感离子通道抑制剂阿米洛利(Ami)预处理后膜电位的振幅、达峰时间等。结果 pH(6.5、6.2、5.9)酸刺激使髓核致炎大鼠神经元膜电位振幅一过性增加,Ost浓度依赖性的抑制膜电位振幅变化(P<0.05),20g·L-1和50g·L-1Ost强于Ami(P<0.05,P<0.05),复合应用Ami可增强Ost抑制效果(P<0.05)。结论 Ost抑制酸刺激诱发的髓核致炎大鼠DRG神经元去极化,增强炎症环境中神经元的抗酸能力。Aim To investigate the effect of osthole （Ost） on the acid-stimulated change of mambrane potential （MP） in dorsal root ganglia neurons separated from rats with inflammatory hyperalgesia following application of nucleus pulposus（NP）.Methods Inflammatory hyperalgesia rat model was induced by application of NP on left lumbar 5 dorsal root ganglion （DRG）.Neurons were separated and labeled by DiBAC4 （3） on postoperative d 3.The dynamic variation of fluoresence intensiy（FI,reflection of MP） and time to peak （Tpeak） evoked by acid at different pH values and after pretreatment of Ost or amiloride（Ami） were recorded.Results Acid at pH（5.9,6.2,6.5） significantly induced depolarizational change of MP.The ele-vated MP was concentration-dependently inhibited by the pre-treatment of Ost（P0.05）,while the effects of 20g·L-1 （P0.05） and 50g· L-1 （P0.05） Ost were more potent than Ami.Combination of Ost and Ami produced stronger reduction of the elevated MP than Ost alone （P0.05）.Conclusion Osthole inhibits the acid-stimulated change of DRG neuron＇s MP of rats with NP-induced hyperalgesia,potentiating the anti-acid property of neurons in inflammatory surroundings.

关 键 词：蛇床子素 细胞膜电位 pH 酸敏感离子通道 阿米洛利 背根神经节 髓核 

分 类 号：R-332[医药卫生] R284.1