Elevation of cortical C26:0 due to the decline of peroxisomal β-oxidation potentiates amyloid β generation and spatial memory deficits via oxidative stress in diabetic rats

As a kind of medicine which can also be used as food,Alpinia oxyphyllaMiq. has a long clinical history in China. A variety of studies demonstrated the significant neuroprotective activity effects of chloroform (CF) extract from the fruits ofAlpinia oxyphylla.In order to further elucidate the possible mechanisms of CF extract which mainly contains sesquiterpenes with neuroprotection on the cognitive ability, mice were injected with Aβ1−42and later with CF in this study. The results showed that the long-term treatment of CF enhanced the cognitive performances in behavior tests, increased activities of glutathione peroxidase (GSH-px) and decreased the level of malondialdehyde (MDA), acetylcholinesterase (AChE), and amyloid-β(Aβ), and reversed the activation of microglia, degeneration of neuronal acidophilia, and nuclear condensation in the cortex and hippocampus. These results demonstrate that CF ameliorates learning and memory deficits by attenuating oxidative stress and regulating the activation of microglia and degeneration of neuronal acidophilia to reinforce cholinergic functions.

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Spatial memory deficits and oxidative stress damage following exposure to lipopolysaccharide in a rodent model of Parkinson's disease

Neuroscience Research ◽

10.1016/j.neures.2011.05.016 ◽

2011 ◽

Vol 71 (1) ◽

pp. 35-43 ◽

Cited By ~ 30

Author(s):

Lucian Hritcu ◽

Alin Ciobica ◽

Marius Stefan ◽

Marius Mihasan ◽

Lavinia Palamiuc ◽

...

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Spatial Memory ◽

Memory Deficits ◽

Rodent Model ◽

Stress Damage ◽

And Oxidative Stress

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Enteromorpha prolifera Extract Improves Memory in Scopolamine-Treated Mice via Downregulating Amyloid-β Expression and Upregulating BDNF/TrkB Pathway

Antioxidants ◽

10.3390/antiox9070620 ◽

2020 ◽

Vol 9 (7) ◽

pp. 620

Author(s):

Seung Yeon Baek ◽

Fu Yi Li ◽

Da Hee Kim ◽

Su Jin Kim ◽

Mee Ree Kim

Keyword(s):

Oxidative Stress ◽

Amyloid Β ◽

Memory Deficits ◽

Morris Water Maze Test ◽

Marker Enzyme ◽

Enteromorpha Prolifera ◽

Memory Impairments ◽

Traditional Remedies ◽

Preliminary Study ◽

The Brain

Enteromorpha prolifera, a green alga, has long been used in food diets as well as traditional remedies in East Asia. Our preliminary study demonstrated that an ethyl acetate extract of Enteromorpha prolifera (EAEP) exhibited the strongest antioxidant activity compared to ethanol or water extracts. Nonetheless, there has been no report on the effect of EAEP on memory impairment due to oxidative damage. This study investigated whether EAEP could attenuate memory deficits in an oxidative stress-induced mouse model. EAEP was orally administered (50 or 100 mg/kg body weight (b.w.)) to mice and then scopolamine was administered. The oral administration of EAEP at 100 mg/kg b.w. significantly restored memory impairments induced by scopolamine, as evaluated by the Morris water maze test, and the passive avoidance test. Further, EAEP upregulated the protein expression of BDNF, p-CREB, p-TrkB, and p-Akt. Moreover, EAEP downregulated the expression of amyloid-β, tau, and APP. The regulation of cholinergic marker enzyme activities and the protection of neuronal cells from oxidative stress-induced cell death in the brain of mice via the downregulation of amyloid-β and the upregulation of the BDNF/TrkB pathway by EAEP suggest its potential as a pharmaceutical candidate to prevent neurodegenerative diseases.

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Chronic epigallocatechin-3-gallate ameliorates learning and memory deficits in diabetic rats via modulation of nitric oxide and oxidative stress

Behavioural Brain Research ◽

10.1016/j.bbr.2011.06.007 ◽

2011 ◽

Vol 224 (2) ◽

pp. 305-310 ◽

Cited By ~ 54

Author(s):

Tourandokht Baluchnejadmojarad ◽

Mehrdad Roghani

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Learning And Memory ◽

Memory Deficits ◽

Diabetic Rats ◽

Learning And Memory Deficits ◽

And Oxidative Stress

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

Arquivos de Neuro-Psiquiatria ◽

10.1590/0004-282x20160065 ◽

2016 ◽

Vol 74 (6) ◽

pp. 482-488 ◽

Cited By ~ 13

Author(s):

Wenna Liang ◽

Xiaoyang Zhao ◽

Jinping Feng ◽

Fenghua Song ◽

Yunzhi Pan

Keyword(s):

Oxidative Stress ◽

Ursolic Acid ◽

Memory Impairment ◽

Tumor Necrosis ◽

Therapeutic Strategy ◽

Antioxidant Activities ◽

Neuroprotective Effect ◽

Amyloid Β ◽

Memory Deficits ◽

Memory Impairments

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.

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