芍药苷抑制大鼠小脑浦肯野细胞对急性缺氧的功能反应  

Paeoniflorin inhibits functional responses of rat cerebellar Purkinje cells to acute hypoxia insult

作　　者：任颖鸽 谭晓丽[2] 陈静[2] 张静[2] 杜永平[1] 张月萍[2] 

机构地区：[1]第四军医大学西京医院全军中医内科中心,陕西西安710032 [2]第四军医大学西京医院儿科脑发育研究室,陕西西安710032

出　　处：《中国病理生理杂志》2015年第4期664-668,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30871029);第四军医大学西京医院助推计划(No.XJZT10T07)

摘　　要：目的:研究芍药苷(paeoniflorin,Pae)对大鼠小脑浦肯野细胞(Purkinje cells,PCs)急性缺氧电生理反应的影响。方法:采用全细胞膜片钳记录法,记录大鼠小脑PCs膜电位、兴奋性和平行纤维(parallel fibre,PF)-PC兴奋性突触后电流(excitatory postsynaptic currents,EPSCs),观察急性缺氧和芍药苷对上述电生理功能的影响。结果:缺氧后PCs首先表现为短暂的超极化,继之以短暂的去极化和持续超极化,芍药苷完全阻断了PCs的缺氧性超极化,并使PCs缺氧性去极化的幅度减小,持续时间缩短;缺氧上调了PCs兴奋性,芍药苷对缺氧引起的PCs的高兴奋性无显著影响;急性缺氧引起了PF-PC EPSCs的长时程抑制(long-term depression,LTD);芍药苷可部分逆转缺氧引起的PF-PC EPSCs衰减。结论:芍药苷显著减轻了大鼠小脑PCs的缺氧反应,可能增强了PCs对急性缺氧的耐受性。AIM：To investigate the effects of paeoniflorin （ Pae） on the functional responses induced by acute hypoxic insult in the rat cerebellar Purkinje cells （ PCs） .METHODS：The whole-cell patch clamp was used for the intra-cellular recording of PCs in the rat cerebellar slices to evaluate the changes of membrane potential, the excitability of PCs, and the parallel fibre （ PF）-PC excitatory postsynaptic currents （ EPSCs） upon acute hypoxic insult alone or with the pre-sence of Pae.RESULTS：PCs showed an initial hyperpolarization followed by brief depolarization and long lasting post-hy-poxia hyperpolarization after hypoxia exposure.Pae completely blocked hypoxia-induced hyperpolarization and decreased the amplitude and the duration of hypoxic depolarization.Hypoxia up-regulated the excitability of rat PCs.Pae didn’t show any significant effect on the hypoxia-induced hyperexcitability in PCs.Acute hypoxia induced long-term depression （ LTD） in rat cerebellar PF-PC EPSCs, and Pae partially reversed hypoxia-induced depression in PF-PC EPSCs.CONCLUSION：Pae significantly suppresses hypoxia-induced responses in rat PCs and probably increases the tolerance of rat PCs to acute hypoxia.

关 键 词：芍药苷 缺氧 浦肯野细胞 膜电位 突触传递 

分 类 号：R363[医药卫生—病理学] R338.8[医药卫生—基础医学]