Ginkgo biloba Extract EGb761 Protects Against Mitochondrial Dysfunction in Platelets and Hippocampi in Ovariectomized Rats
 
   

Ginkgo biloba Extract EGb761 Protects Against Mitochondrial
Dysfunction in Platelets and Hippocampi in Ovariectomized Rats

This section is compiled by Frank M. Painter, D.C.
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   Frankp@chiro.org
 
   

FROM:   Platelets 2010 (Feb);   21 (1):   53-9

Shi C, Fang L, Yew DT, Yao Z, Xu J

Department of Anatomy,
Zhongshan School of Medicine,
Sun Yat-Sen University,
Guangzhou, Guangdong 510080, China


Ginkgo biloba seems to protect against post-menopausal degenerative brain disease through it's protective effects on the mitochondria. Estrogen withdrawal seems to accelerate the decline of mitochondria populations within the brain, and in this study, Ginkgo was shown to protect against that.

Using ovariectomized middle-aged rats to mimic the post-menopausal pathophysiological changes in women, we have previously demonstrated that estrogen withdrawal and age-related decrease in the functional reserve of mitochondria might co-operate to induce persistent mitochondrial dysfunction, which may be critical in inducing degenerative processes in the brain later in post-menopausal women. The standardized Ginkgo biloba extract EGb761 has long been considered a natural antioxidant. More recently it has also proposed to have direct protective effects on the mitochondria. In this work, effects of EGb761 on mitochondrial function in platelets and hippocampi of ovariectomized and sham-operated rats were investigated. It was found that EGb761 protected against the decrease of cytochrome c oxidase (COX) activity, mitochondrial ATP (adenosine-5'-triphosphate) content and mitochondrial glutathione (GSH) content in both platelets and hippocampi of ovariectomized rats, suggesting its peripheral and central effects against estrogen withdrawal-induced degeneration. In contrast, in sham-operated rats, EGb761 increased mitochondrial GSH content in platelets but failed to show similar effect on hippocampi, suggesting that EGb761 may help to enhance the functional reserve of mitochondria, but this effect was limited to the outside of the central nervous system. EGb761 displayed similar effects on platelets and hippocampi of ovariectomized rats but showed differential effects on platelets and hippocampi of sham-operated rats, possibly because estrogen withdrawal induced an increase of blood brain barrier (BBB) permeability. Therefore, while EGb761's effect may be limited to the outside of the nervous system under normal physiological conditions, EGb761 may be a potential protective agent against central neurodegeneration in post-menopausal women.


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