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

Abstract

Objective: Increasing evidence demonstrates that oxidative stress and inflammatory are involved in amyloid β (Aβ)-induced memoryimpairments. Ursolic acid (UA), a triterpenoid compound, has potent anti-inflammatory and antioxidant activities. However, it remainsunclear whether UA attenuates Aβ-induced neurotoxicity. Method: The aggregated Aβ25-35was intracerebroventricularly administered tomice. Results: We found that UA significantly reversed the Aβ25-35-induced learning and memory deficits. Our results indicated that oneof the potential mechanisms of the neuroprotective effect was attenuating the Aβ25-35-induced accumulation of malondialdehyde (MDA)and depletion of glutathione (GSH) in the hippocampus. Furthermore, UA significantly suppressed the upregulation of IL-1β, IL-6, andtumor necrosis-α factor levels in the hippocampus of Aβ25-35-treated mice. Conclusion: These findings suggest that UA prevents memoryimpairment through amelioration of oxidative stress, inflammatory response and may offer a novel therapeutic strategy for the treatmentof Alzheimer’s disease.