4.7 Article

Inhibitory Effect of Lychee Seed Saponins on Apoptosis Induced by Aβ25-35 through Regulation of the Apoptotic and NF-κB Pathways in PC12 Cells

期刊

NUTRIENTS
卷 9, 期 4, 页码 -

出版社

MDPI
DOI: 10.3390/nu9040337

关键词

Alzheimer's disease; lychee seed saponins; A beta(25-35); PC12 cells; apoptosis; NF-kappa B

资金

  1. Science and Technology Planning Project of Sichuan Province, China [2008SZ0050, LZ-LY-38]
  2. Educational Commission of Sichuan Province, China [10ZA035, 2016-JYT015]
  3. Key Development Program of Southwest Medical University [2014ZD-010, 2014QN-043]

向作者/读者索取更多资源

Neuronal apoptosis plays a critical role in the pathogenesis of Alzheimer's disease (AD). Previous studies have shown that lychee seed saponins (LSS), isolated and extracted from traditional Chinese medicine lychee seeds, possess many beneficial activities including anti-oxidation, anti-diabetes, anti-AD, etc. In the present study, we established an in vitro neuronal apoptotic model of PC12 cells induced by A beta(25-35) and studied the effect of LSS on apoptosis by the methods of Hoechst 33342/propidium iodide (PI) fluorescence double staining, Annexin V/PI double staining, and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). We also investigated the effects of LSS on mitochondria membrane potential, the expressions of Bcl-2 and Bax proteins, and the mRNA expression and the nuclear translocation of NF-kappa Bp65 in PC12 cells. The results showed that LSS markedly inhibited apoptosis, improved the mitochondria membrane potentials, upregulated the expression of Bcl-2 protein, downregulated the expression of Bax protein, and decreased the mRNA expression and nuclear translocation of NF-kappa Bp65 in PC12 cells. The study demonstrated that LSS significantly inhibited apoptosis induced by A beta(25-35) via regulation of the apoptotic and NF-kappa B pathways in PC12 cells. Therefore, LSS has the potential to be developed as a novel agent or nutrient supplement for the prevention and/or treatment of AD.

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