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

Objective: Increasing evidence demonstrates that oxidative stress and inflammatory are involved in amyloid beta (A beta)-induced memory impairments. Ursolic acid (UA), a triterpenoid compound, has potent anti-inflammatory and antioxidant activities. However, it remains unclear whether UA attenuates A beta-induced neurotoxicity. Method: The aggregated A beta(25.35) was intracerebroventriculary administered to mice. Results: We found that UA significantly reversed the A beta(25-35) induced learning and memory deficits. Our results indicated that one of the potential mechanisms of the neuroprotective effect was attenuating the A beta(25-35)-induced accumulation of malondialdehyde (MDA) and depletion of glutathione (GSH) in the hippocampus. Furthermore, UA significantly suppressed the upregulation of IL-1 beta, IL-6, and tumor necrosis-alpha factor levels in the hippocampus of A beta(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.