PRUNETIN ATTENUATES D-GALACTOSE-INDUCED BRAIN AGING VIA INHIBITING AMYLOID-Β AND TAU PROTEIN AGGREGATION

Abstract

The objective of this investigation was to assess the effect of prunetin in D-galactose-induced brain aging in rats and its regulating mechanisms. D-galactose (200 mg kg-1 body wt.) was given orally daily for 45 days to accelerate aging, and prunetin (10, 20,40, and 80 µg kg-1 body wt. respectively) was administered orally. The anti-oxidant and anti-brain aging activities of prunetin in serum were measured by the estimation of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) levels and brain tissues were measured by western blot analysis and histopathological studies. Prunetin therapy decreases elevated levels of glucose, C-reactive protein, cholesterol, and triglyceride levels in the D-galactose-induced rats. D-galactose suppresses the levels of superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity in rats; these levels were elevated by treating with prunetin. Malondialdehyde levels were elevated in D-galactose-induced rats. Prunetin significantly decreases the malondialdehyde levels in rat brain tissue. Prunetin decreases mitochondrial dysfunction induced by D-galactose, by improving the activities of Na+K+-ATPase and acetylcholinesterase enzyme activity. Western blot analysis results showed that the degree of brain tissue damage was significantly reduced by prunetin. The results of our study indicated that prunetin treatment reduced oxidative stress by exerting a protective effect against D-galactose-induced aging in rats, by significantly decreasing amyloid - β and tau protein levels in the brain tissue. Prunetin exhibits anti-oxidant activity by increasing anti-oxidant enzymes.