Ginkgo biloba leaf extract reverses amyloid beta-peptide-induced isoprostane production in rat brain in vitro.

Isoprostanes are prostaglandin (PG) isomers generated from oxygen radical peroxidation of arachidonic acid, which are reliable markers of membrane oxidative damage. Aging is characterized by an imbalance between the generation of reactive oxygen species and antioxidant detoxification pathways. Ginkgo biloba leaf extract is reputed as a neuroprotective antioxidant agent. We have tested the effects of a Ginkgo biloba extract {containing 24.1 % flavonoids and 181 % terpene lactones [bilobalide (0.542 %), ginkgolide A (0.570 %), ginkgolide B (0.293 %), ginkgolide C (0.263 %), and ginkgolide J (0.138 %)]} on the production of 8-iso-PGF2alpha from rat brain synaptosomes obtained from young (3 months old) or aged (12 and 24 months old) rats, both in the basal state and after oxidative stress induced by either hydrogen peroxide or amyloid beta-peptide. Our findings show that Ginkgo biloba extract pretreatment is able to completely reverse both basal and hydrogen peroxide-stimulated isoprostane production (IC50 of 81.92 microM and 31.89 microM, respectively). Amyloid beta-peptide-induced isoprostane production was also inhibited, both in young and aged rats, to a level even lower than that in unstimulated synaptosomes. This suggests that the oxygen radical scavenging properties of the Ginkgo biloba extract are fully effective in young, as well as in old rats, showing a greater inhibition of isoprostane production in the latter.