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Published on: July 25, 2011
Neuroprotection by bilobalide in ischemia: improvement of mitochondrial function
T M Schwarzkopf1, S Hagl, G P Eckert
1Pharmakologisches Institut für Naturwissenschaftler, Goethe Universittit Frankfurt am Main, Germany.
Die Pharmazie
|August 9, 2013
Summary
Bilobalide, from Ginkgo biloba, protects the brain from stroke damage by improving mitochondrial function and reducing harmful glutamate release. This neuroprotective effect was observed in mice following ischemic injury.
Area of Science:
- Neuroscience
- Pharmacology
- Mitochondrial Biology
Background:
- Bilobalide, a Ginkgo biloba constituent, exhibits neuroprotective effects.
- The precise mechanism underlying bilobalide's neuroprotection is not fully understood.
Purpose of the Study:
- To investigate the neuroprotective mechanisms of bilobalide.
- To evaluate bilobalide's effects on mitochondrial function and neurotransmitter release during ischemic stroke.
Main Methods:
- Transient middle cerebral artery occlusion (tMCAO) model in mice.
- Assessment of brain damage using TTC staining.
- Microdialysis to measure glutamate and glucose levels in the ischemic striatum.
- Ex vivo analysis of mitochondrial respiration and permeability transition pore opening.
Main Results:
- Bilobalide significantly reduced brain damage post-tMCAO.
- Bilobalide perfusion decreased ischemia-induced glutamate release by 70% without affecting glucose levels.
- Mitochondrial respiratory capacity, particularly Complex I, was improved by bilobalide treatment.
- Bilobalide reversed tMCAO-induced mitochondrial swelling.
Conclusions:
- Bilobalide confers neuroprotection by mitigating ischemia-induced mitochondrial dysfunction.
- The drug's mechanism involves reversing mitochondrial changes, leading to reduced glutamate excitotoxicity.
