天然产物研究与开发 ›› 2019, Vol. 31 ›› Issue (1): 49-54.doi: 10.16333/j.1001-6880.2019.1.008

• 研究论文 • 上一篇    下一篇

四氢紫堇萨明对Aβ25-35诱导AD细胞模型凋亡的影响及其机制研究

姚兵1,侯斌1,李文燕1,位庚2,陈檬1,李辉欣1,宋燕飞1,梁俊清1*   

  1. 1河北省中西医结合医药研究院,石家庄 050035;2石家庄市第二医院,石家庄 050051
  • 出版日期:2019-01-28 发布日期:2019-01-28
  • 基金资助:

    国家自然科学基金青年基金(81503231);河北省科技计划(162777284)

Effects and mechanism of tetrahydrocorysamine on apoptosis of AD cell model induced by Aβ25-35

YAO Bing 1,HOU Bin1,LI Wen-yan1,WEI Geng2,CHEN Meng1,LI Hui-xin1,SONG Yan-fei 1,LIANG Jun-qing1*   

  1. 1Hebei Pharmaceutical Research Institute of Integrated Chinese and Western Medicine,Shijiazhuang 050035,China; 2The Second Hospital of Shijiazhuang,Shijiazhuang 050051,China
  • Online:2019-01-28 Published:2019-01-28

摘要: 探讨四氢紫堇萨明(SQZJSM)对阿尔茨海默病(AD)细胞模型凋亡的影响及作用机制。采用Aβ25-35诱导神经细胞PC-12损伤建立AD细胞模型,通过流式细胞仪检测凋亡率,高通量高内涵分析系统观察细胞核形态并检测线粒体膜电位(MMP)变化,Western blot法检测凋亡相关蛋白的表达。结果显示,SQZJSM可改善模型细胞受损的细胞核形态,同时显著减少模型细胞凋亡率和胞质Cyt C含量,上调MMP,降低Bax、Cleaved-Caspase 3、Cleaved-Caspase 9蛋白表达,增加Bcl-2、p-Akt/T-Akt表达(P<0.05);PI3K/AKT抑制剂LY294002可阻断SQZJSM对模型细胞的上述改善作用。以上结果表明四氢紫堇萨明可显著改善Aβ25-35诱导的AD细胞模型凋亡,其机制可能与激活PI3K/Akt信号通路调控内源性线粒体凋亡途径相关。

关键词: 延胡索, 四氢紫堇萨明, A&beta, 25-35, PC-12, 线粒体凋亡, Akt

Abstract: To explore the effect of tetrahydrocorysamine on the apoptosis of Alzheimers disease (AD) cell model and its possible mechanism.Alzheimer's disease cell model was established by Aβ25-35 inducing PC-12 cells.Flow cytometry was used to measure the apoptosis rate,high-throughput and high-content analysis system was used to observe the nuclear morphological changes and detect mitochondrial membrane potential (MMP) changes,the expression of apoptosis-related protein was detected by Western blot.The results showed that SQZJSM can improve the damaged nuclear morphology of model cells,and significantly reduce the apoptosis rate and Cyt C level in the cytoplasm,up-regulate the level of MMP,decrease the expression of Bax,Cleaved-Caspase3,Cleaved-Caspase 9 protein,and increase the level of Bcl-2,p-Akt/T-Akt (P <0.05);PI3K/AKT inhibitor LY294002 can block the improvement of SQZJSM on model cells.The above results indicate that tetrahydrocorysamine can significantly reduce the apoptosis rate of AD cell model induced by Aβ25-35,which may be related to the activation of PI3K/Akt signaling pathway to regulate endogenous mitochondrial apoptosis.

Key words: corydalis, tetrahydrocorysamine, Aβ25-35, PC-12, mitochondrial apoptosis, Akt

中图分类号: 

R965.1