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    Vincamine Alleviates Amyloid‑β 25–35 Peptides‑induced Cytotoxicity in PC12 Cells

    Jianfeng Han1, Qiumin Qu1, Jin Qiao1, Jie Zhang2 Corresponding author

    1. 1Department of Neurology, The First Clinical Hospital of Xian Jiaotong University, Xian 710061, China.
    2. 2Institute of Liver Disease, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R, China.

    CORRESPONDENCE

    Jie Zhang

    Institute of Liver Disease, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R, China.

    jzhang_shtcm@sina.com

    Received: 28-08-2015; Revised: 14-10-2015.

    Volume 13, Issue 49 · pp. 123–128 · PUBLISHED 6 January 2017 · DOI: 10.4103/0973-1296.196309

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objective: Vincamine is a plant alkaloid used clinically as a peripheral vasodilator that increases cerebral blood flow and oxygen and glucose utilization by neural tissue to combat the effect of aging. The main purpose of the present study is to investigate the influence of vincamine on amyloid‑β 25–35 (Aβ25–35) induced cytotoxicity, to gain a better understanding of the neuroprotective effects of this clinically used anti‑Alzheimer’s disease drug. Materials and Methods: Oxidative stress was assessed by measuring malondialdehyde, glutathione, and superoxide dismutase (SOD) levels. Cell viability was assessed by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay. Cell apoptosis detection was performed using an Annexin‑V‑FITC Apoptosis Detection Kit. The production of reactive oxygen species (ROS) was determined using an ROS Assay Kit. Western blot detection was carried out to detect the protein expression. Results: Our studies showed that pretreatment with vincamine could reduce Aβ25–35 induced oxidative stress. Vincamine markedly inhibited cell apoptosis dose‑dependently. More importantly, vincamine increased the phosphatidylinositol‑3 kinase (PI3K)/Akt and Bcl‑2 family protein ratios on preincubation with cells for 2 h. Conclusion: Above observation led us to assume that one possible mechanism of vincamine protects Aβ25‑35‑induced cell death could be through upregulation of SOD and activation of the PI3K/Akt pathway.

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      Han, J., Qu, Q., Qiao, J., & Zhang, J. (2017). Vincamine Alleviates Amyloid‑β 25–35 Peptides‑induced Cytotoxicity in PC12 Cells. Pharmacognosy Magazine, 13(49), 123–128. https://doi.org/10.4103/0973-1296.196309