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首页> 外文期刊>Nutrients >Inhibitory Effect of Lychee Seed Saponins on Apoptosis Induced by Aβ 25-35 through Regulation of the Apoptotic and NF-κB Pathways in PC12 Cells
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Inhibitory Effect of Lychee Seed Saponins on Apoptosis Induced by Aβ 25-35 through Regulation of the Apoptotic and NF-κB Pathways in PC12 Cells

机译:荔枝籽皂苷通过调节PC12细胞凋亡和NF-κB途径抑制Aβ25-35诱导的细胞凋亡

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摘要

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 Aβ 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-κBp65 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-κBp65 in PC12 cells. The study demonstrated that LSS significantly inhibited apoptosis induced by Aβ 25-35 via regulation of the apoptotic and NF-κB 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.
机译:神经元凋亡在阿尔茨海默氏病(AD)的发病机理中起着至关重要的作用。先前的研究表明,从中药荔枝种子中提取和提取的荔枝种子皂苷具有许多有益的活性,包括抗氧化,抗糖尿病,抗AD等。在本研究中,我们建立了Aβ25-35诱导PC12细胞的体外神经元凋亡模型,并通过Hoechst 33342 /碘化丙啶(PI)荧光双重染色,膜联蛋白V / PI双重染色和末端脱氧核苷酸转移酶(TdT)的方法研究了LSS对凋亡的影响)介导的dUTP缺口末端标记(TUNEL)。我们还研究了LSS对PC12细胞中线粒体膜电位,Bcl-2和Bax蛋白表达以及NF-κBp65mRNA表达和核转运的影响。结果表明,LSS能够显着抑制PC12细胞凋亡,提高线粒体膜电位,上调Bcl-2蛋白表达,下调Bax蛋白表达,降低NF-κBp65的mRNA表达和核转运。研究表明,LSS通过调节PC12细胞的凋亡和NF-κB途径,显着抑制Aβ25-35诱导的凋亡。因此,LSS有潜力被开发为预防和/或治疗AD的新型药物或营养补充剂。

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