Wenna Liang1, Xiaoyang Zhao1, Jinping Feng1, Fenghua Song2, Yunzhi Pan3. 1. The Third People's Hospital, Liaocheng, Department of Neurology, Shandong , China, The Third People's Hospital of Liaocheng, Department of Neurology, Shandong, China; 2. The Third People's Hospital, Liaocheng, Department of Pharmacy, Shandong , China, The Third People's Hospital of Liaocheng, Department of Pharmacy, Shandong, China; 3. The Third Affiliated Hospital, Qiqihar Medical University, Department of Neurology, Heilong Jiang , China, The Third Affiliated Hospital of Qiqihar Medical University, Department of Neurology, Heilong Jiang, China.
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 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.
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.
Authors: Xoan Thi Le; Hien Thu Nguyen; Tai Van Nguyen; Hang Thi Nguyet Pham; Phuong Thi Nguyen; Khoi Minh Nguyen; Ba Van Nguyen; Kinzo Matsumoto Journal: Evid Based Complement Alternat Med Date: 2021-06-30 Impact factor: 2.629