scholarly journals Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer’s Disease

Molecules ◽  
2021 ◽  
Vol 26 (10) ◽  
pp. 3011
Author(s):  
Ines ELBini-Dhouib ◽  
Raoudha Doghri ◽  
Amenallah Ellefi ◽  
Imen Degrach ◽  
Najet Srairi-Abid ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Histopathological Analysis ◽  
Protective Effects ◽  
Inflammatory Cytokine Production ◽  
Beneficial Effects ◽  
Model Of Alzheimer’S Disease ◽  
Natural Polyphenol ◽  
Anti Inflammatory

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases leading to dementia. Despite research efforts, currently there are no effective pharmacotherapeutic options for the prevention and treatment of AD. Recently, numerous studies highlighted the beneficial effects of curcumin (CUR), a natural polyphenol, in the neuroprotection. Especially, its dual antioxidant and anti-inflammatory properties attracted the interest of researchers. In fact, besides its antioxidant and anti-inflammatory properties, this biomolecule is not degraded in the intestinal tract. Additionally, CUR is able to cross the blood–brain barrier and could therefore to be used to treat neurodegenerative pathologies associated with oxidative stress, inflammation and apoptosis. The present study aimed to assess the ability of CUR to induce neuronal protective and/or recovery effects on a rat model of neurotoxicity induced by aluminum chloride (AlCl3), which mimics the sporadic form of Alzheimer’s disease. Our results showed that treatment with CUR enhances pro-oxidant levels, antioxidant enzymes activities and anti-inflammatory cytokine production and decreases apoptotic cells in AlCl3-exposed hippocampus rats. Additionally, histopathological analysis of hippocampus revealed the potential of CUR in decreasing the hallmarks in the AlCl3-induced AD. We also showed that CUR post-treatment significantly improved the behavioral, oxidative stress and inflammation in AlCl3-exposed rats. Taken together, our data presented CUR as a nutraceutical potential through its protective effects that are more interesting than recovery ones in sporadic model of AD.

Berberine-Albumin Nanoparticles: Preparation, Thermodynamic Study and Evaluation Their Protective Effects Against Oxidative Stress in Primary Neuronal Cells as a Model of Alzheimer’s Disease

2021 ◽  
Vol 17 (6) ◽  
pp. 1088-1097
Author(s):  
Yaohui Zhang ◽  
Lixiang Wang ◽  
Guichen Li ◽  
Jianyuan Gao
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antioxidant Activity ◽  
Molecular Docking ◽  
Morphological Changes ◽  
Neuronal Cultures ◽  
Protective Effects ◽  
Cellular Assays ◽  
Model Of Alzheimer’S Disease

Berberine has shown an outstanding antioxidant activity, however the low bioavailability limits its applications in pharmaceutical platforms. Therefore, in this paper, after fabrication of the berberine-HSA nanoparticles by desolvation method, they were well characterized by TEM, SEM, DLS, and FTIR techniques. Afterwards the interaction of HSA and the berberine was evaluated by molecular docking analysis. Finally, the antioxidant activity of the berberine-HSA nanoparticles against H2O2-induced oxidative stress in cultured neurons as a model of AD was evaluated by cellular assays. The results showed that the prepared berberine-HSA nanoparticles have a spherical-shaped morphology with a size of around 100 nm and zeta potential value of −31.84 mV. The solubility value of nanoparticles was calculated to be 40.27%, with a berberine loading of 19.37%, berberine entrapment efficiency of 70.34%, and nanoparticles yield of 88.91%. Also, it was shown that the berberine is not significantly released from HSA nanoparticles within 24 hours. Afterwards, molecular docking investigation revealed that berberine spontaneously interacts with HSA through electrostatic interaction. Finally, cellular assays disclosed that the pretreatment of neuronal cultures with berberine-HSA nanoparticles decreased the H2O2-stimulated cytotoxicity and relevant morphological changes and enhanced the CAT activity. In conclusion, it can be indicated that the nanoformulation of the berberine can be used as a promising platform for inhibition of oxidative damage-induced Alzheimer’s disease (AD).

scholarly journals Sinapic Acid Alleviates Oxidative Stress and Neuro-Inflammatory Changes in Sporadic Model of Alzheimer’s Disease in Rats

2020 ◽  
Vol 10 (12) ◽  
pp. 923
Author(s):  
Vandna Verma ◽  
Devendra Singh ◽  
Reeta KH
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Sinapic Acid ◽  
Neuronal Loss ◽  
Protective Effects ◽  
Cholinergic Dysfunction ◽  
Model Of Alzheimer’S Disease ◽  
Neuro Inflammation

The role of oxidative stress, neuro-inflammation and cholinergic dysfunction is already established in the development of Alzheimer’s disease (AD). Sinapic acid (SA), a hydroxylcinnamic acid derivative, has shown neuro-protective effects. The current study evaluates the neuro-protective potential of SA in intracerebroventricular streptozotocin (ICV-STZ) induced cognitive impairment in rats. Male Wistar rats were bilaterally injected with ICV-STZ. SA was administered intragastrically once daily for three weeks. Rats were divided into sham, ICV-STZ, STZ + SA (10 mg/kg), STZ + SA (20 mg/kg) and SA per se (20 mg/kg). Behavioral tests were assessed on day 0 and 21 days after STZ. Later, rats were sacrificed for biochemical parameters, pro-inflammatory cytokines, choline acetyltransferase (ChAT) expression and neuronal loss in the CA1 region of the hippocampus. The results showed that SA 20 mg/kg significantly (p < 0.05) improved cognitive impairment as assessed by Morris water maze and passive avoidance tests. SA 20 mg/kg reinstated the altered levels of GSH, MDA, TNF-α and IL-1β in the cortex and hippocampus. STZ-induced decreased expression of ChAT and neuronal loss were also significantly (p < 0.05) improved with SA. Our results showed that SA exhibits neuro-protection against ICV-STZ induced oxidative stress, neuro-inflammation, cholinergic dysfunction and neuronal loss, suggesting its potential in improving learning and memory in patients of AD.

scholarly journals Chronic Oral Palmitoylethanolamide Administration Rescues Cognitive Deficit and Reduces Neuroinflammation, Oxidative Stress, and Glutamate Levels in A Transgenic Murine Model of Alzheimer’s Disease

2020 ◽  
Vol 9 (2) ◽  
pp. 428 ◽  
Author(s):  
Sarah Beggiato ◽  
Maria Cristina Tomasini ◽  
Tommaso Cassano ◽  
Luca Ferraro
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficit ◽  
Lipid Mediator ◽  
Beneficial Effects ◽  
Model Of Alzheimer’S Disease ◽  
Tnf Α ◽  
Transgenic Murine Model ◽  
Factor Α

N-palmitoylethanolamide (PEA) is a lipid mediator belonging to the class of the N-acylethanolamine. Products containing PEA, also in ultramicronized formulation (um-PEA), are already licensed for use in humans for its analgesic and anti-inflammatory properties, and demonstrated high safety and tolerability. Preclinical studies indicate that PEA, especially in the ultramicronized form, could be a potential therapeutic agent for Alzheimer’s disease (AD). In this study, we evaluated the neuroprotective and antioxidant effects of chronic (three months) um-PEA administration in an animal model of AD (3×Tg-AD mice). For translation purposes, the compound has been orally administered. Cognitive performance as well as biochemical markers [(interleukin-16 (IL-16) and tumor necrosis factor-α (TNF-α)] levels, reactive oxygen species (ROS) production, synaptophysin and glutamate levels) have been evaluated at the end of um-PEA treatment. The results indicate that orally administered um-PEA was adsorbed and distributed in the mice brain. The chronic treatment with um-PEA (100 mg/kg/day for three months) rescued cognitive deficit, restrained neuroinflammation and oxidative stress, and reduced the increase in hippocampal glutamate levels observed in 3×Tg-AD mice. Overall, these data reinforce the concept that um-PEA exerts beneficial effects in 3×Tg-AD mice. The fact that PEA is already licensed for the use in humans strongly supports its rapid translation in clinical practice.

Impact of Cerebral Radiofrequency Exposures on Oxidative Stress and Corticosterone in a Rat Model of Alzheimer’s Disease

2020 ◽  
Vol 73 (2) ◽  
pp. 467-476 ◽  
Author(s):  
Marc Bouji ◽  
Anthony Lecomte ◽  
Christelle Gamez ◽  
Kelly Blazy ◽  
Anne-Sophie Villégier
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Model Of Alzheimer’S Disease

Beneficial effects of quetiapine in a transgenic mouse model of Alzheimer's disease

2009 ◽  
Vol 30 (8) ◽  
pp. 1205-1216 ◽  
Author(s):  
Jue He ◽  
Huanmin Luo ◽  
Bin Yan ◽  
Yingxin Yu ◽  
Haitao Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Beneficial Effects ◽  
Model Of Alzheimer’S Disease
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