NATURAL PRODUCT RESEARCH AND DEVELOPMENT ›› 2019, Vol. 31 ›› Issue (1): 49-54.doi: 10.16333/j.1001-6880.2019.1.008

• Article • Previous Articles     Next Articles

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

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

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