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The effect of Ginkgo biloba extract on central nervous system

         Ginkgo is Ginkgo Branch, ginkgo species, also known as white fruit trees, ancient Permian relict plant, a "living fossil". To GBE for the raw material preparation, widely used in medicines, health products, food additives, functional beverages, cosmetics and other fields. The product is one of the most successful case of modern science and technology to develop herbal medicine (a traditional Chinese medicine).

 

          Some European countries the use of its treatment of central nervous system lesions, if national treatment of cerebral vascular insufficiency and tinnitus as a non-prescription drugs, Germany ginkgo biloba to treat dementia, France for the treatment of mental retardation syndrome. Ginkgo biloba compound have been developed to inhibit the cellular organization of amyloid deposition, can improve cognitive function, improve memory, for the treatment and age-related cognitive impairment or memory loss. Plant extracts to alleviate the symptoms of cognitive impairment, although the ginkgo biloba extract (EGb) is the most extensive, but its mechanism of action of the central nervous system (CNS) are poorly understood, is now on in recent years related to the EGb on the CNS The study can be summarized as the following four aspects.


          To Neuronal damage:
          Recent studies have focused on a variety of acute and chronic neurological degenerative diseases, EGb the role of oxidative stress. However, the exact mechanism of the oxidative stress induced denaturation process remains controversial. Researchers have used different in vitro model to simulate the negative impact of oxidative stress to the cell viability and to evaluate the protective properties of the pharmacological effects of substances. In the oxidative stress response by hydrogen peroxide-induced rat model of schizophrenia, we tested the influence of EGb cerebellar neurons. Hydrogen peroxide to increase the number of dead neurons in a time dependent manner, given in the pre-treatment of EGb, may significantly delay the above reaction. Oxidative stress, or 60min after the application of EGb, then the effect greatly reduced. In general, the oxidative stress in neuronal death process of apoptosis in the pathogenesis of neurodegenerative played an important role. Ni et al studied the effects of EGb on oxidative stress-induced brain neuronal apoptosis. Neurons exposed to hydroxyl radicals in neurons pre-processing with EGb mortality. Has confirmed that EGb contains Flavonoids can reduce the generation of reactive oxygen species, suggesting that EGb may be by directly scavenging hydroxyl radicals, oxidative stress induced cell death to produce a protective effect.
 

     To Brain ischemia:
     Brain ischemia, thrombosis, spasm, or low blood pressure causes will lead to a series of vascular and metabolic changes, and these changes are difficult to model in experimental animals. Currently the most widely used ischemia model ligation in gerbils with unilateral carotid artery. Normal neurological parameters as an indicator of research, whether it is oral or intraperitoneal administration of EGb in experimental animals can make the normalization of mitochondrial respiration, and cerebral edema, correct ion disorder and restore the overall function. Another group of gerbils experiment, taking EGb14 days before on both sides of the forebrain ischemia can prevent the occurrence of cerebral ischemia, a significant increase in the number of the protected neurons. These results suggest that: of EGb treatment can prevent progression of ischemic neurons. Cerebral ischemia experiments show that neurons protective effect may be attributed to of ginkgolide the antagonistic platelet-activating factor (PAF) activity.
 
      
     Studies have shown that application of ginkgolide A and B, brain blood flow can increase 50% to 100%. This effect is similar to papaverine and inhibiting phosphodiesterase so that cAMP increased the role that speed up the heart rate and increased myocardial oxygen consumption, and ginkgolide A and B can significantly inhibit the secretion of cortisol and corticosterone, in order to prevent neurotoxic effects of excessive corticosteroids.

 

     That EGb on the protection of the ischemic neurons, the material basis of clear free radicals and antioxidant flavonoids with anti-PAF and antioxidant activity of ginkgolide and bilobalide.

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