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Published on: November 26, 2015
Ginkgo Biloba Extract Attenuates Oxidative Stress and Apoptosis in Mouse Cochlear Neural Stem Cells
1Department of Pharmacy, Eye and ENT Hospital of Fudan University, 83 Fenyang Road, Shanghai, 200031, China.
Abstract:
In the organ or Corti, oxidative stress could result in damage to the hearing, and neural stem cells (NSCs) hold great therapeutic potential in treating hearing loss. Ginkgo biloba extract (GBE) has been widely shown to exhibit anti-oxidative and anti-apoptotic effects in treatments of neural damage and disorder. Using hydrogen peroxide to induced oxidative stress as a model, we investigated the anti-oxidative role of GBE in isolated mouse cochlear NSCs. GBE treatment was found to significantly promote viability of NSCs, by markedly attenuating hydrogen peroxide induced oxidative stress. In addition, this anti-oxidative function of GBE was also able to prevent mitochondrial depolarization and subsequent apoptosis. Moreover, the anti-apoptotic role of GBE was mediated by antagonizing the intrinsic mitochondrial apoptotic pathway, where GBE could reverse the changes in key intrinsic apoptosis pathway factors including Bcl-2, Bax, and Caspase-3. Our data provided the first report on the beneficial role of GBE in protecting cochlear NSCs, by attenuating oxidative stress triggered intrinsic apoptosis, therefore supporting the potential therapeutic value of GBE in preventing oxidative stress-related hearing loss. Copyright © 2016 John Wiley & Sons, Ltd.
Insights
Ginkgo biloba extract protects hearing stem cells from oxidative stress. This extract shows therapeutic potential for preventing hearing loss by reducing cell death and damage.
Area of Science:
- Oto-neuroscience
- Stem cell biology
- Pharmacology
Background:
- Oxidative stress in the organ of Corti can lead to hearing damage.
- Neural stem cells (NSCs) offer therapeutic potential for hearing loss.
- Ginkgo biloba extract (GBE) has known antioxidant and anti-apoptotic properties.
Purpose of the Study:
- To investigate the protective effects of GBE against oxidative stress in mouse cochlear NSCs.
- To elucidate the mechanisms underlying GBE's protective actions.
Main Methods:
- Induction of oxidative stress using hydrogen peroxide in isolated mouse cochlear NSCs.
- Assessment of NSC viability and apoptosis.
- Analysis of mitochondrial membrane potential and key apoptosis-related factors (Bcl-2, Bax, Caspase-3).
Main Results:
- GBE significantly enhanced NSC viability by attenuating hydrogen peroxide-induced oxidative stress.
- GBE prevented mitochondrial depolarization and subsequent apoptosis.
- GBE's anti-apoptotic effect was mediated by antagonizing the intrinsic mitochondrial pathway, normalizing Bcl-2, Bax, and Caspase-3 levels.
Conclusions:
- GBE demonstrates a beneficial role in protecting cochlear NSCs from oxidative stress.
- GBE mitigates oxidative stress-induced intrinsic apoptosis in cochlear NSCs.
- GBE holds therapeutic potential for preventing hearing loss associated with oxidative stress.
