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Neuroprotection against cobalt chloride-induced cell apoptosis of primary cultured cortical neurons by salidroside
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  • 作者:1. Jiangsu Key Laboratory of Neuroregeneration ; Nantong University ; 19 Qixiu Road ; Nantong ; 226001 Jiangsu ; People’s Republic of China
  • 关键词:Salidroside – Cobalt chloride – Hypoxia – Cell apoptosis – Cortical neurons
  • 刊名:Molecular and Cellular Biochemistry
  • 出版年:2011
  • 出版时间:August 2011
  • 年:2011
  • 卷:354
  • 期:1-2
  • 页码:161-170
  • 全文大小:638.4 KB
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  • 作者单位:http://www.springerlink.com/content/m024777r57t77536/
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Biochemistry
    Medical Biochemistry
    Oncology
    Cardiology
  • 出版者:Springer Netherlands
  • ISSN:1573-4919
文摘
Salidroside, a phenol glycoside of plant origin, has been documented to possess a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by different insults. To provide further insights into the neuroprotective functions peculiar to salidroside, this study used primary cultured cortical neurons of rats as a cell model to examine whether salidroside was able to prevent against cell damage after exposure to cobalt chloride (CoCl2), a hypoxia-inducing agent. The data from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test, Hoechst33342 staining, terminal deoxynucleotidyl transferase dUTP-mediated nicked end labeling assay, and Bax/Bcl-2 ratio analysis indicated that salidroside pretreatment attenuated hypoxia-induced apoptotic cell death of primary cultured cortical neurons in a dose-dependent manner. Moreover, preliminary exploration of the possible mechanisms suggested that the protective effects of salidroside, shown in our experimental setting, might probably be mediated by enhancing the expression of hypoxia-inducible factor-1α, alleviating the increase of intracellular reactive oxygen species levels, and inhibiting over-expression of nuclear factor-kappa B protein.

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