Ginkgo biloba extract protected against brain tissue hypoxic damage in vitro.
The ginkgolides and bilobalide were responsible for the antihypoxic activity of
the extract (38, 39). Ginkgolides A and B have been shown to protect rat
hippocampal neurons against ischaemic damage, which may be due to their
ability to act as antagonists to receptors for platelet-activating factor (PAF) (40–
42).
In vivo studies. Oral administration of G. biloba extract protected rats against
induced cerebral ischaemia (43–45). Intravenous perfusion of a G. biloba extract
prevented the development of multiple cerebral infarction in dogs injected with
fragments of an autologous clot into a common carotid artery (46). These data
suggest that G. biloba extract, administered after clot formation, may have some
beneficial effects on acute cerebral infarction or ischaemia caused by embolism
(1). Other experiments demonstrated that animals treated with G. biloba extract
survived under hypoxic conditions longer than did untreated controls (47, 48).
Longer survival was due not only to significant improvements in cerebral blood
flow, but also to an increase in the level of glucose and ATP (44, 48–50). Other
studies have shown that a G. biloba extract devoid of ginkgolides but containing
bilobalide had protective activity when administered intraperitoneally to mice
with induced hypobaric hypoxia (51, 52). Intravenous infusion of G. biloba
extract significantly increased pial arteriolar diameter in cats (53) and improved