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Gingko biloba extract (EGb 761) attenuates the focal cerebral ischemic injury-induced decrease in astrocytic
1Department of Anatomy, College of Veterinary Medicine and Research Institute of Life Science, Gyeongsang National University, Jinju 660-701, South Korea. pokoh@gnu.ac.kr
The American Journal of Chinese Medicine
|September 10, 2011
Summary
Ginkgo biloba extract EGb 761 protects against brain injury by maintaining levels of phosphoprotein enriched in astrocytes 15 (PEA-15) and its phosphorylated forms during ischemic events.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Focal cerebral ischemic injury can lead to neuronal damage.
- Phosphoprotein enriched in astrocytes 15 (PEA-15) plays a role in regulating cell apoptosis.
- EGb 761, a Ginkgo biloba extract, exhibits neuroprotective properties.
Purpose of the Study:
- To investigate the effect of EGb 761 on PEA-15 expression and phosphorylation in a rat model of cerebral ischemic injury.
- To determine if EGb 761 can prevent the reduction of PEA-15 and its phosphorylated forms following middle cerebral artery occlusion (MCAO).
Main Methods:
- Adult male rats underwent MCAO to induce ischemic injury.
- Rats were pretreated with either vehicle or EGb 761 (100 mg/kg).
- Proteomic and Western blot analyses were used to assess PEA-15 and phospho-PEA-15 (Ser 104, Ser 116) levels in cerebral cortices 24 hours post-MCAO.
Main Results:
- MCAO injury significantly reduced the expression of PEA-15 and its phosphorylated forms.
- EGb 761 pretreatment effectively prevented the MCAO-induced decrease in PEA-15 expression.
- EGb 761 attenuated the reduction in phospho-PEA-15 (Ser 104) and phospho-PEA-15 (Ser 116) caused by ischemic injury.
Conclusions:
- EGb 761 maintains PEA-15 expression and phosphorylation during cerebral ischemic injury.
- The neuroprotective effect of EGb 761 against cerebral ischemia may be mediated through the regulation of PEA-15 phosphorylation.
- Preserving PEA-15 phosphorylation is crucial for its anti-apoptotic function and neuroprotection.
