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Updated: Mar 19, 2026
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Ursolic acid attenuates beta-amyloid-induced memory impairment in mice
Wenna Liang1, Xiaoyang Zhao1, Jinping Feng1
1The Third People's Hospital, Liaocheng, Department of Neurology, Shandong , China, The Third People's Hospital of Liaocheng, Department of Neurology, Shandong, China;
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 Aβ25-35 was intracerebroventricularly administered to mice.
Results:
We found that UA significantly reversed the Aβ25-35-induced learning and memory deficits. Our results indicated that one of 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, and tumor necrosis-α factor levels in the hippocampus of Aβ25-35-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.
