黄芪总苷及黄芪甲苷对糖皮质激素诱导老前期小鼠记忆障碍的保护作用及其机制

目的探讨黄芪总苷（Astragaloside，AST）和黄芪甲苷（Astragalus Saponin I，ASI）对氢化可的松（Hydrocortisone，HC）引起小鼠记忆障碍的保护作用及对胞浆钙浓度（[Ca^2＋]i）的影响。方法用HC（4mg·kg^-1，se，21d）建立老前期小鼠学习记忆损伤模型，避暗实验检测小鼠学习记忆功能；Fura-2／AM负载法检测小鼠胸腺细胞和海马神经元突触体[Ca^2＋]i；电镜观察海马神经元的超微结构。结果与HC模型组比较，AST（50mg·kg^-1）和ASI（50mg·kg^-1）能改善小鼠的记忆功能，降低小鼠胸腺细胞和海马神经元突触体[Ca^2＋]i，改善海马神经元的超微结构。结论氢化可的松可明显引起老前期小鼠记忆障碍，AST和ASI能改善小鼠的学习记忆功能，其机制可能与抑制细胞内钙超载有关。

Protective effects of AST and ASI on glucocorticoid-induced mouse memory impairment and its mechanism

Aim To study the protective effects of Astragaloside （ AST ） and Astragalus Saponin I （ ASI ） on glucocorticoid-induced mouse memory impairment, hippocampal neuron intrasynaplosomes [Ca^2＋] i and ultrastructure. Methods Step-Throwgh test was performed to observe the effects of AST and ASI on memory impairment of HC-induced mouse. Using Ca^2＋ sensitive fluorescent indicator （Furo-2） , free intracellular calcium concentration （ [Ca^2＋ ] i ） was measured using double wavelength fluorescence sepeetrophotometer in thymocytes and hippocampal neurons. Electron microscope was used to observe the ultrastructure of hippocampal neurons. Results . HC （4.0 mg· kg-1 ） could induce memory impairment in 20 mon mine. Compared with HC treated group,AST （50mg· kg-1） and ASI （50mg· kg-1 ） were shown to improve their impairment of memory.decreased [ Ca^2＋] i of thymocytes and hippocampal, improved the ultrastructure of hippocampal neurons and inhibited the hippocampal neuron apoptosis. Conclusion AST and ASI could restore memory impairment in HC treated mice. and its mechanism may decrease intracellular calcium concentration in hippocampus and thymocytes and inhibit the hippocampal neuron apoptosis.