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Bilobalide and neuroprotection.

Abstract
In vivo studies have indicated that systemically administered bilobalide, a sesquiterpene trilactone constituent of Ginkgo biloba leaf extracts, can reduce cerebral edema produced by triethyltin, decrease cortical infarct volume in certain stroke models, and reduce cerebral ischemia. In vitro and ex vivo studies indicate that bilobalide has multiple mechanisms of action that may be associated with neuroprotection, including its preservation of mitochondrial ATP synthesis, its inhibition of apoptotic damage induced by staurosporine or by serum-free medium, its suppression of hypoxia-induced membrane deterioration in the brain, and its actions of increasing the expression of the mitochondrial DNA-encoded COX III subunit of cytochrome c oxidase and the ND1 subunit of NADH dehydrogenase. As multiple modes of action may apply to bilobalide, it could be useful in developing therapy for disorders involving cerebral ischemia and neurodegeneration.
AuthorsFrancis V Defeudis
JournalPharmacological research (Pharmacol Res) Vol. 46 Issue 6 Pg. 565-8 (Dec 2002) ISSN: 1043-6618 [Print] Netherlands
PMID12457632 (Publication Type: Journal Article, Review)
Chemical References
  • Cyclopentanes
  • Diterpenes
  • Furans
  • Ginkgolides
  • Neuroprotective Agents
  • Plant Extracts
  • bilobalide
Topics
  • Animals
  • Cell Survival (drug effects, physiology)
  • Cerebrovascular Disorders (drug therapy, physiopathology)
  • Cyclopentanes (isolation & purification, pharmacology, therapeutic use)
  • Diterpenes
  • Furans (isolation & purification, pharmacology, therapeutic use)
  • Ginkgo biloba
  • Ginkgolides
  • Humans
  • Neuroprotective Agents (isolation & purification, pharmacology, therapeutic use)
  • Phytotherapy
  • Plant Extracts (isolation & purification, pharmacology, therapeutic use)
  • Plant Leaves

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