人参皂苷Rg1抑制叔丁基过氧化氢诱导的原代大鼠皮层神经元损伤  

Ginsenoside Rg1 protects primary rat cerebrocortical neurons against t-BHP-induced damage in vitro

作　　者：逯丹[1] 舒晓明[1] 张婵娟[1] 赵佳仪 朱丽红[1] 戚仁斌[1] 王华东[1] 陆大祥[1] 

机构地区：[1]暨南大学医学院病理生理学系,暨南大学脑科学研究所,国家中医药管理局重点科研实验室,广东广州510632

出　　处：《中国病理生理杂志》2014年第3期479-485,共7页Chinese Journal of Pathophysiology

基　　金：国家重点基础研究发展计划(973计划)(No.2011CB707501);广州市科技计划项目重大专项(No.11BppZXaa2070006);国家自然科学基金资助项目(No.81371442)

摘　　要：目的:观察人参皂苷Rg1对叔丁基过氧化氢(t-BHP)诱导的原代大鼠皮层神经元损伤的改善作用,并探讨其可能机制。方法:将神经元随机分为正常对照组、10μmol/L t-BHP组及10μmol/L t-BHP+10μmol/L人参皂苷Rg1组,培养24 h。采用MTT检测不同浓度t-BHP处理的神经元活性,神经元三维重建研究神经元平均总纤维长度及总突起数量,免疫荧光检测caspase-3表达水平及免疫印迹方法检测Bcl-2、caspase-3以及磷酸化糖原合成酶激酶3β(pGSK-3β)蛋白表达水平。结果:10μmol/L人参皂苷Rg1能够对抗10μmol/L t-BHP引起的原代大鼠皮层神经元活性水平的降低,并且上调Bcl-2及pGSK-3β蛋白表达量,降低caspase-3活化为cleaved caspase-3的水平(P<0.05)。结论:人参皂苷Rg1可能通过提高GSK-3β自身磷酸化从而增强神经元的抗t-BHP损伤能力。AIM： To observe the effect of ginsenoside Rgl （G-Rgl） on tert-butyl hydroperioxideo （t-BHP）- induced injury in primary rat cerebrocortical neurons and their filaments. METHODS： Primary rat cerebrocortical neurons were randomly divided into normal group, 10 μmol/L t-BHP induction group and 10 μmol/L t-BHP ＋ 10 umol/L G-Rgl treatment group. The MTF assay was used to detect the cell viability under various concentrations of t-BHP. 3D cell recon struction was performed to measure the filament length and number. The protein expression levels of Bcl-2, phosphorylated glycogen synthase kinase 3β （pGSK-3β） and caspase-3 were determined by the methods of immunofluorescence and West era blotting. RESULTS： G-Rgl at concentration of 10 μmo]-/L reversed the decrease in cell viability, increased the pro tein expression level of Bcl-2 and pGSK-3β, and suppressed the activation of caspase-3 in t-BHP induction group （P 〈 0. 05 ）. CONCLUSION： G-Rgl increases the anti-stress ability of the neurons by increasing the pGSK-3β phosphoylation under the condition of t-BHP exposure.

关 键 词：人参皂苷RG1 叔丁基过氧化氢 糖原合成酶激酶3B 

分 类 号：R329.21[医药卫生—人体解剖和组织胚胎学]