Resveratrol (3,5,4'-trihydroxystilbene), a viniferin polyphenolic compound, has been shown to have neuroprotective effects and we tested its possible antioxidant activity in young and aged rat brain, evaluating, in vitro, synaptosomal 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)) production as a marker of oxidative stress. We found that in young rat brain synaptosomes resveratrol perfusion had no effect on basal 8-iso-PGF(2 alpha) production, but quenched to basal levels the increased 8-iso-PGF(2 alpha) production induced by hydrogen peroxide. On the other hand, in aged rats, resveratrol was able to decrease 8-iso-PGF(2 alpha) production both basally and after hydrogen peroxide-induced oxidative stimulus. In conclusion, our findings show that the antioxidant effects of resveratrol in rat brain could play a neuroprotective role in aging, when the increased burden of oxidative stress is faced by defective antioxidant mechanisms.

Resveratrol inhibits isoprostane production in young and aged rat brain.

CHIAVAROLI, Annalisa;BRUNETTI, Luigi;ORLANDO, Giustino;RECINELLA, Lucia;FERRANTE, CLAUDIO;LEONE, Sheila;DI MICHELE, PIERPAOLO;DI NISIO, Chiara;VACCA, Michele
2010-01-01

Abstract

Resveratrol (3,5,4'-trihydroxystilbene), a viniferin polyphenolic compound, has been shown to have neuroprotective effects and we tested its possible antioxidant activity in young and aged rat brain, evaluating, in vitro, synaptosomal 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)) production as a marker of oxidative stress. We found that in young rat brain synaptosomes resveratrol perfusion had no effect on basal 8-iso-PGF(2 alpha) production, but quenched to basal levels the increased 8-iso-PGF(2 alpha) production induced by hydrogen peroxide. On the other hand, in aged rats, resveratrol was able to decrease 8-iso-PGF(2 alpha) production both basally and after hydrogen peroxide-induced oxidative stimulus. In conclusion, our findings show that the antioxidant effects of resveratrol in rat brain could play a neuroprotective role in aging, when the increased burden of oxidative stress is faced by defective antioxidant mechanisms.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/175826
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