EGb761 protects hydrogen peroxide-induced death of spinal cord neurons through inhibition of intracellular ROS production and modulation of apoptotic regulating genes

Xiaoyan Jiang, Baoming Nie, Saili Fu, Jianguo Hu, Lan Yin, Lin Lin, Xiaofei Wang, Peihua Lu, Xiao Ming Xu

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

The present study was conducted to investigate whether Ginkgo biloba extract (EGb) 761 could protect spinal cord neurons from H2O2-induced toxicity. In primary spinal cord neurons isolated from embryonic day 14 rats, H2O2 administration resulted in a significant decrease in the survival of spinal cord neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and Hoechst 33342 n clear staining showed that these cells die by apoptosis. Such neuronal death, however, was significantly reversed by EGb761 in a dose-dependent manner. Moreover, a marked increase in intracellular free radical generation was found after the H2O2 administration which could be reversed almost completely by EGb761, indicating that inhibition of free radical generation is an important mechanism of the anti-apoptosis action of EGb761. Finally, treatment of cells with H2O2 for 12 h reduced the expression of Bcl-2, an anti-apoptotic gene, by 70% but showed no effect on the level of Bax, a pro-apoptotic gene. EGb76 treatment, however, significantly reversed H2O2- induced reduction of Bcl-2 expression and inhibited Bax expression by 2.3-fold. Thus, our study provided evidence showing that the protective effect of EGb761 on spinal cord neuronal apoptosis after oxidative stress is mediated, at least in part, by its anti-oxidative action and regulation of apoptosis-related genes Bcl-2 and Bax.

Original languageEnglish (US)
Pages (from-to)103-113
Number of pages11
JournalJournal of Molecular Neuroscience
Volume38
Issue number2
DOIs
StatePublished - Jun 1 2009

Fingerprint

Hydrogen Peroxide
Spinal Cord
Neurons
Apoptosis
Genes
Free Radicals
bcl-2 Genes
DNA Nucleotidylexotransferase
Ginkgo biloba extract 761
Oxidative Stress
Staining and Labeling

Keywords

  • Apoptosis
  • EGb761
  • Hydrogen peroxide
  • Neuroprotection
  • Oxidative stress
  • Spinal cord neurons

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

EGb761 protects hydrogen peroxide-induced death of spinal cord neurons through inhibition of intracellular ROS production and modulation of apoptotic regulating genes. / Jiang, Xiaoyan; Nie, Baoming; Fu, Saili; Hu, Jianguo; Yin, Lan; Lin, Lin; Wang, Xiaofei; Lu, Peihua; Xu, Xiao Ming.

In: Journal of Molecular Neuroscience, Vol. 38, No. 2, 01.06.2009, p. 103-113.

Research output: Contribution to journalArticle

Jiang, Xiaoyan ; Nie, Baoming ; Fu, Saili ; Hu, Jianguo ; Yin, Lan ; Lin, Lin ; Wang, Xiaofei ; Lu, Peihua ; Xu, Xiao Ming. / EGb761 protects hydrogen peroxide-induced death of spinal cord neurons through inhibition of intracellular ROS production and modulation of apoptotic regulating genes. In: Journal of Molecular Neuroscience. 2009 ; Vol. 38, No. 2. pp. 103-113.
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AB - The present study was conducted to investigate whether Ginkgo biloba extract (EGb) 761 could protect spinal cord neurons from H2O2-induced toxicity. In primary spinal cord neurons isolated from embryonic day 14 rats, H2O2 administration resulted in a significant decrease in the survival of spinal cord neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and Hoechst 33342 n clear staining showed that these cells die by apoptosis. Such neuronal death, however, was significantly reversed by EGb761 in a dose-dependent manner. Moreover, a marked increase in intracellular free radical generation was found after the H2O2 administration which could be reversed almost completely by EGb761, indicating that inhibition of free radical generation is an important mechanism of the anti-apoptosis action of EGb761. Finally, treatment of cells with H2O2 for 12 h reduced the expression of Bcl-2, an anti-apoptotic gene, by 70% but showed no effect on the level of Bax, a pro-apoptotic gene. EGb76 treatment, however, significantly reversed H2O2- induced reduction of Bcl-2 expression and inhibited Bax expression by 2.3-fold. Thus, our study provided evidence showing that the protective effect of EGb761 on spinal cord neuronal apoptosis after oxidative stress is mediated, at least in part, by its anti-oxidative action and regulation of apoptosis-related genes Bcl-2 and Bax.

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