Ursolic acid attenuates beta-amyloid-induced memory impairment in mice

Ácido ursólico atenua a perda de memória induzida por beta-amilóide em ratos

ABSTRACT

Objective

Increasing evidence demonstrates that oxidative stress and inflammatory are involved in amyloid β (Aβ)-induced memory impairments. Ursolic acid (UA), a triterpenoid compound, has potent anti-inflammatory and antioxidant activities. However, it remains unclear whether UA attenuates Aβ-induced neurotoxicity.

Method

The aggregated Aβ_25-35 was intracerebroventricularly administered to mice.

Results

We found that UA significantly reversed the Aβ_25-35-induced learning and memory deficits. Our results indicated that one of the potential mechanisms of the neuroprotective effect was attenuating the Aβ_25-35-induced accumulation of malondialdehyde (MDA) and depletion of glutathione (GSH) in the hippocampus. Furthermore, UA significantly suppressed the upregulation of IL-1β, IL-6, and tumor necrosis-α factor levels in the hippocampus of Aβ_25-35-treated mice.

Conclusion

These findings suggest that UA prevents memory impairment through amelioration of oxidative stress, inflammatory response and may offer a novel therapeutic strategy for the treatment of Alzheimer’s disease.

amyloid; memory; oxidative stress; ursolic acid