Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 38, Issue 2, Pages 103-113Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-008-9140-0
Keywords
Hydrogen peroxide; Spinal cord neurons; Oxidative stress; EGb761; Apoptosis; Neuroprotection
Categories
Funding
- 973 Project [2003CB515302]
- Shanghai Science and Technology Developing Foundation [00JC14021]
- Shanghai Educational Committee Technology Foundation [99ZD08]
- NIH [NS36350, NS50243, NS52290]
Ask authors/readers for more resources
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 nuclear 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available