scholarly journals (-)-cis-Carveol, a Natural Compound, Improves β-Amyloid-Peptide 1-42-Induced Memory Impairment and Oxidative Stress in the Rat Hippocampus

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Lucian Hritcu ◽  
Razvan Stefan Boiangiu ◽  
Mayara Castro de Morais ◽  
Damião Pergentino de Sousa
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Amyloid Peptide ◽  
Radial Arm Maze ◽  
Reference Drug ◽  
Y Maze ◽  
Group A ◽  
Biochemical Analyses

Alzheimer’s disease (AD) could be considered a multifactorial neurodegenerative disorder characterized by the accumulation of the β-amyloid-peptide (Aβ) within the brain leading to cognitive deficits, oxidative stress, and neuroinflammation. The present work was carried out to investigate the neuroprotective effect of (-)-cis-carveol (1% and 3%, for 21 days) against the β-amyloid-peptide 1-42- (Aβ1-42-) induced AD. Twenty-five rats were divided into five groups (n=5/group): the first group—control (sham-operated); the second group—Aβ1-42 (1 mM) that received donepezil treatment (5 mg/kg, as the positive reference drug in the Y-maze and the radial arm maze tests); the third group—Aβ1-42 (1 mM); the fourth and fifth groups—Aβ1-42 (1 mM) that received (-)-cis-carveol treatment groups (1% and 3%). The results of this study demonstrated that (-)-cis-carveol improved Aβ1-42-induced memory deficits examined by using Y-maze and radial arm maze in vivo tests. Also, the biochemical analyses of the hippocampus homogenates showed that (-)-cis-carveol reduced hippocampal oxidative stress caused by Aβ1-42. Our results suggested that the use of (-)-cis-carveol may be suitable for decreasing AD-related symptoms.

scholarly journals Alleviation of Memory Deficit by Bergenin via the Regulation of Reelin and Nrf-2/NF-κB Pathway in Transgenic Mouse Model

2021 ◽  
Vol 22 (12) ◽  
pp. 6603
Author(s):  
Bushra Shal ◽  
Adnan Khan ◽  
Ashraf Ullah Khan ◽  
Rahim Ullah ◽  
Gowhar Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Neuroprotective Effect ◽  
Annexin V ◽  
Memory Deficit ◽  
Y Maze ◽  
Spatial Memory Deficit ◽  
Aβ Aggregation ◽  
Ft Ir ◽  
Reelin Signaling

The present study aims to determine the neuroprotective effect of Bergenin against spatial memory deficit associated with neurodegeneration. Preliminarily, the protective effect of Bergenin was observed against H2O2-induced oxidative stress in HT-22 and PC-12 cells. Further studies were performed in 5xFAD Tg mouse model by administering Bergenin (1, 30 and 60 mg/kg; orally), whereas Bergenin (60 mg/kg) significantly attenuated the memory deficit observed in the Y-maze and Morris water maze (MWM) test. Fourier transform-infrared (FT-IR) spectroscopy displayed restoration of lipids, proteins and their derivatives compared to the 5xFAD Tg mice group. The differential scanning calorimeter (DSC) suggested an absence of amyloid beta (Aβ) aggregation in Bergenin-treated mice. The immunohistochemistry (IHC) analysis suggested the neuroprotective effect of Bergenin by increasing Reelin signaling (Reelin/Dab-1) and attenuated Aβ (1–42) aggregation in hippocampal regions of mouse brains. Furthermore, IHC and western blot results suggested antioxidant (Keap-1/Nrf-2/HO-1), anti-inflammatory (TLR-4/NF-kB) and anti-apoptotic (Bcl-2/Bax/Caspase-3) effect of Bergenin. Moreover, a decrease in Annexin V/PI-stained hippocampal cells suggested its effect against neurodegeneration. The histopathological changes were reversed significantly by Bergenin. In addition, a remarkable increase in antioxidant level with suppression of pro-inflammatory cytokines, oxidative stress and nitric oxide production were observed in specific regions of the mouse brains.

In vivo neuroprotective effect of L-carnitine against oxidative stress in maple syrup urine disease

2011 ◽  
Vol 26 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Caroline Mescka ◽  
Tarsila Moraes ◽  
Andrea Rosa ◽  
Priscila Mazzola ◽  
Bruna Piccoli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Maple Syrup Urine Disease ◽  
Neuroprotective Effect ◽  
Maple Syrup ◽  
Urine Disease

scholarly journals Attenuation of Spatial Memory in 5xFAD Mice by Halting Cholinesterases, Oxidative Stress and Neuroinflammation Using a Cyclopentanone Derivative

2020 ◽  
Vol 13 (10) ◽  
pp. 318
Author(s):  
Rahim Ullah ◽  
Gowhar Ali ◽  
Nisar Ahmad ◽  
Muhammad Akram ◽  
Geeta Kumari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Inflammatory Cytokines ◽  
In Vivo Studies ◽  
Cholinesterase Inhibition ◽  
Rt Pcr ◽  
Y Maze ◽  
5Xfad Mice

Alzheimer’s disease (AD) is an irreversible and chronic neurological disorder that gradually destroys memory and thinking skills. The research study was designed to investigate the underlying molecular signaling involved in the neuroprotective effects of cyclopentanone derivative i.e., 2-(hydroxyl-(3-nitrophenyl)methyl)cyclopentanone (3NCP) as a therapeutic agent for AD. In this study, In vivo studies were carried out on a well-known 5xFAD mice model using different behavioural test models such as open field, rotarod, Morris water maze (MWM), and Y-maze tests. Furthermore, in vitro cholinesterase inhibition activity assays were carried out. The frontal cortex (FC) and hippocampus (HC) homogenates were tested for the levels/activities of cholinesterases, glutathione (GSH), glutathione S-transferase (GST), and catalase. Furthermore, the hippocampal expression of inflammatory cytokines was observed via RT-PCR and western blot. The results of in vivo studies show an enhancement in the learning behavior. The 3NCP treatment reduced latency time in MWM and Y-maze tests, also increase spontaneous alternation indicate significant effect of 3NCP on memory. Furthermore, open field and rotarod studies revealed that 3NCP does not cause motor coordination deficit. The results of the in vitro studies revealed that the IC50 values of the 3NCP against acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were 16.17 and 20.51 µg/mL, respectively. This decline in AChE and BChE was further supported by ex vivo studies. Further, the 3NCP mitigates the GSH level, GST, and catalase activities in HC and FC. The mRNA and protein expression of inflammatory cytokines (IL-1β, IL-6, TNF-α) markedly declined in RT-PCR and western blotting. The results of the current study conclusively demonstrate that 3NCP reduces oxidative stress and mitigates neuroinflammation in 5xFAD mice, implying that 3NCP may be a potential therapeutic candidate for AD treatment in the future.

The Neuroprotective Effect of Picroside II from Hu-Huang-Lian against Oxidative Stress

2007 ◽  
Vol 35 (04) ◽  
pp. 681-691 ◽  
Author(s):  
Ting Li ◽  
Jian-Wen Liu ◽  
Xiao-Dong Zhang ◽  
Ming-Chuan Guo ◽  
Guang Ji
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Active Constituent ◽  
Sod Activity ◽  
Picroside Ii ◽  
Pre Treatment

Picroside II is an active constituent extracted from the traditional Chinese medicine (TCM) Hu-Huang-Lian. To evaluate the neuroprotective effect of picroside II, PC12 cells were treated with glutamate in vitro and male ICR mice were treated with AlCl 3in vivo. Pre-treatment of PC12 cells with picroside II could enhance the cell viability and decrease the level of intracellular reactive oxygen species (ROS) induced by glutamate. By DNA fragmentation and flow cytometry assay, picroside II (1.2 mg/ml) significantly prevented glutamate-induced cell apoptosis. In the animal study, amnesia was induced in mice by AlCl 3 (100 mg/kg/d, i.v.). Pricroside II, at the dose of 20 and 40 mg/kg/d (i.g.), markedly ameliorated AlCl 3-induced learning and memory dysfunctions and attenuated AlCl 3-induced histological changes. This was associated with the significant increased superoxide dismutase (SOD) activity in the brain of experimental mice. All these results indicated that picroside II possessed the therapeutic potential in protecting against neurological injuries damaged by oxidative stress.

scholarly journals Cognitive Facilitation and Antioxidant Effects of an Essential Oil Mix on Scopolamine-Induced Amnesia in Rats: Molecular Modeling of In Vitro and In Vivo Approaches

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1519 ◽  
Author(s):  
Razvan Stefan Boiangiu ◽  
Ion Brinza ◽  
Monica Hancianu ◽  
Ilkay Erdogan Orhan ◽  
Gokcen Eren ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Essential Oil ◽  
Rat Model ◽  
Active Site ◽  
Gas Chromatography Mass Spectrometry ◽  
Active Site Residues ◽  
Reference Drug ◽  
Brain Oxidative Stress

The present study investigated the capability of an essential oil mix (MO: 1% and 3%) in ameliorating amnesia and brain oxidative stress in a rat model of scopolamine (Sco) and tried to explore the underlying mechanism. The MO was administered by inhalation to rats once daily for 21 days, while Sco (0.7 mg/kg) treatment was delivered 30 min before behavioral tests. Donepezil (DP: 5 mg/kg) was used as a positive reference drug. The cognitive-enhancing effects of the MO in the Sco rat model were assessed in the Y-maze, radial arm maze (RAM), and novel object recognition (NOR) tests. As identified by gas chromatography–mass spectrometry (GC–MS), the chemical composition of the MO is comprised by limonene (91.11%), followed by γ-terpinene (2.02%), β-myrcene (1.92%), β-pinene (1.76%), α-pinene (1.01%), sabinene (0.67%), linalool (0.55%), cymene (0.53%), and valencene (0.43%). Molecular interactions of limonene as the major compound in MO with the active site of butyrylcholinesterase (BChE) was explored via molecular docking experiments, and Van der Waals (vdW) contacts were observed between limonene and the active site residues SER198, HIS438, LEU286, VAL288, and PHE329. The brain oxidative status and acetylcholinesterase (AChE) and BChE inhibitory activities were also determined. MO reversed Sco-induced memory deficits and brain oxidative stress, along with cholinesterase inhibitory effects, which is an important mechanism in the anti-amnesia effect. Our present findings suggest that MO ameliorated memory impairment induced by Sco via restoration of the cholinergic system activity and brain antioxidant status.

scholarly journals Protective Activity of Esculetin Against 3-Nitropropionic Acid Induced Neurotoxicity Via Scavenging Reactive Oxygen Species in Male Wistar Rats

2017 ◽  
Vol 9 (5) ◽  
Author(s):  
Arpita Karandikar ◽  
Sumathi Thangarajan
Keyword(s):  
Oxidative Stress ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Neuroprotective Activity ◽  
Protein Carbonyls ◽  
Rat Striatum ◽  
Nitropropionic Acid ◽  
3 Nitropropionic Acid

Huntington’s disease (HD) is a devastating neurodegenerative disorder with no cure till date. Many genetic or chemically induced models have been developed in rodents to study the disease. 3-Nitropropionic (3-NP) acid is a well-known neurotoxin to induce Huntington’s disease (HD) in rodents. It replicates the pathology of HD by causing oxidative stress. Esculetin is a natural compound, a coumarin, known to have neuroprotective effect in a mouse model of Parkinson’s disease. In the present study, the neuroprotective effect of esculetin on 3-NP induced oxidative stress in rat striatum was determined by behavioral and biochemical parameters. Rats were induced with 3-NP (10mg/kg) intraperitoneally for 14 days and rats induced with 3-NP were treated with esculetin (25mg/kg and 50mg/kg) for 14 days. Esculetin attenuated the behaviour of rats in morris water maze, open field, forced swim, narrow beam walk and grip strength test. Biochemical effect of esculetin was also studied on oxidative stress markers, SDH and acetylcholinesterase. Esculetin treatment alleviated the increased values of acetylcholinesterase, protein carbonyls and lipid peroxidation. On treatment with esculetin, we observed that the levels of SOD, GSH, catalase, glutathione peroxidase, SDH were increased. The present study shows that the antioxidant activity of esculetin may be responsible for its neuroprotective activity against 3- nitropropionic acid induced neurotoxicity in rats

scholarly journals Behavioral, Biochemical and Histopathological effects of Standardised Pomegranate extract with Vinpocetine, Propolis or Cocoa in a rat model of Parkinson’s disease

2020 ◽  
Author(s):  
Azza A. Ali ◽  
Mona M. Kamal ◽  
Mona G. Khalil ◽  
Shimaa A. Ali ◽  
Hemat A. Elariny ◽  
...  
Keyword(s):  
Rat Model ◽  
Caspase 3 ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Acetylcholinesterase Activity ◽  
Brain Regions ◽  
Y Maze ◽  
Tnf Α ◽  
Locomotor Activities ◽  
Histopathological Effects

AbstractIntroductionParkinsonism is a neurodegenerative disorder. Pomegranate (POM) has been previously shown to have a dopaminergic neuroprotective effect against Parkinsonism.ObjectiveThe aim of the current study is to compare the efficacy of POM, vinpocetine, Propolis, Cocoa or L-dopa using RT-induced Parkinsonism rat model.MethodsRats were divided into seven groups; one normal and five RT model groups. One of the RT (2.5 mg/kg sc) groups served as non-treated parkinsonism model whereas the others were treated with either L-dopa (10 mg/kg PO) or with POM (150 mg/kg PO) together with each of the following; vinpocetine (VIN) (20 mg/kg PO), Propolis (300 mg/kg PO), Cocoa (24 mg/kg PO). Motor and cognitive performances were examined using three tests (catalepsy, open-field, Y-maze). Striatal dopamine, norepinephrine, serotonin, acetylcholinesterase, GABA, Glutamate, GSK 3B, BDNF levels were assessed as well as MDA, SOD, TAC, IL-1β, TNF-α, iNOs and caspase-3. Also, histopathological examinations of different brain regions were determined.ResultsTreatment with L-dopa alone or with all POM combination groups alleviated the deficits in locomotor activities, cognition, monoamine levels, acetylcholinesterase activity, oxidative stress, and inflammatory markers as well as caspase-3 expression induced by RT.ConclusionCombinations of POM with each of VIN, Propolis or Cocoa have a promising disease-modifying antiparkinsonian therapy even without being given as an adjuvant to L-dopa.

Neuroprotective effect of lacosamide on cognitive dysfunction in Streptozotocin induced Alzheimer disease

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Fatma Sobhy Ibrahim ◽  
Lobna Fouad Abdel-Aziz ◽  
Wesam Mostafa Elbakly ◽  
Nesreen Hamdy El Gayar
Keyword(s):  
Alzheimer Disease ◽  
Antiepileptic Drug ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Mrna Level ◽  
Memory Loss ◽  
Control Group ◽  
Histone Deacetylase Inhibition ◽  
Significant Prolongation ◽  
Y Maze

Abstract Alzheimer disease (AD) is a chronic and progressive neurodegenerative disorder characterized by memory loss and cognition impairment. A link has been established between AD and epilepsy sharing multiple mechanisms and pathogenesis. Similar Hippocampal changes have been found between both diseases. Choosing antiepileptic drug in AD patient represent a great a challenge especially with increase seizure risk in AD patients. Lacosamide, antiepileptic drug, was reported to have a neuroprotective effect in animal models and a histone deacetylase inhibition activity. This study was designed to investigate the potential effect of chronic lacosamide treatment in Streptozotocin induced AD in male Wistar rats. Methods AD animal model was induced with single bilateral intracerebroventricular injection of STZ (3 mg/kg) on day one. Lacosamide (30 mg/kg orally, once daily) was administrated for 21 days. Cognitive function assessment was done with Morris Water Maze (MWM) and Y Maze tasks. APP and MAPT mRNA level were measured. Results ICV-STZ caused significant prolongation in Escape latency time and reduction in time spent in target quadrant in MWM and reduction in spontaneous alteration ratio in Y Maze compared to control group. STZ induced Up-regulation in Amyloid precursor protein and Microtubule associated protein tau gene expression. Chronic Lacosamide treatment attenuated STZ induced cognitive impairment and mitigated APP and MAPT induced expression with STZ. Conclusion Lacosamide has a neuroprotective effect against STZ induced cognitive deficits ameliorating Aβ and Tau pathology.

Oral Supplements of Ginkgo biloba Extract Alleviate Neuroinflammation, Oxidative Impairments and Neurotoxicity in Rotenone-Induced Parkinsonian Rats

2020 ◽  
Vol 21 (12) ◽  
pp. 1259-1268
Author(s):  
Nema A. Mohammed ◽  
Heba M. Abdou ◽  
Mona A. Tass ◽  
Manal Alfwuaires ◽  
Ashraf M. Abdel-Moneim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Ginkgo Biloba ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Radical Scavenging ◽  
Ginkgo Biloba Extract ◽  
Albino Rats ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants

Background: Ginkgo biloba extract (GbE) is known to contain several bioactive compounds and exhibits free radical scavenging activity. Parkinson's Disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons and is associated with oxidative stress, neuroinflammation and apoptosis. Objective: The current study aimed to investigate the neuroprotective effect of GbE in a rat model of PD induced by rotenone (ROT; a neurotoxin). Methods: Twenty-four male albino rats were randomly divided into four groups of six rats each: normal control, GbE treated, toxin control (ROT treated) and GbE+ROT group. Results:: Oral administration of ROT (2.5 mg/kg b.w.) for 50 days caused an increased generation of lipid peroxidation products and significant depletion of reduced glutathione, total thiol content and activities of enzymatic antioxidants, i.e., superoxide dismutase and glutathione peroxidase in the brains of treated rats. Furthermore, ROT caused an elevation in acetylcholinesterase, interleukin-1β, interleukin- 6 and tumor necrosis factor-α and a significant reduction in dopamine in the stratum and substantia nigra. Immunohistochemical results illustrated that ROT treatment reduced the expression of tyrosine hydroxylase (TH). GbE treatment (150 mg/kg b.w./day) significantly reduced the elevated oxidative stress markers and proinflammatory cytokines and restored the reduced antioxidant enzyme activities, DA level and TH expression. These results were confirmed by histological observations that clearly indicated a neuroprotective effect of GbE against ROT-induced PD. Conclusion: GbE mitigated ROT-induced PD via the inhibition of free-radical production, scavenging of ROS, and antioxidant enhancement.

scholarly journals Amyloid-Beta Peptide, Oxidative Stress and Inflammation in Alzheimer's Disease: Potential Neuroprotective Effects of Omega-3 Polyunsaturated Fatty Acids

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
S. C. Dyall
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
The Elderly ◽  
Amyloid Peptide ◽  
Omega 3 ◽  
Neuroprotective Effects ◽  
Beta Peptide ◽  
The Brain

Alzheimer's disease is the most common form of dementia in the elderly and is a progressive neurodegenerative disorder characterised by a decline in cognitive function and also profound alterations in mood and behaviour. The pathology of the disease is characterised by the presence of extracellular amyloid peptide deposits and intracellular neurofibrillary tangles in the brain. Although many hypotheses have been put forward for the aetiology of the disease, increased inflammation and oxidative stress appear key to be features contributing to the pathology. The omega-3 polyunsaturated fats, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) have well-characterised effects on inflammation and may have neuroprotective effects in a number of neurodegenerative conditions including Alzheimer's disease. The aims of this paper are to review the neuroprotective effects of EPA and DHA in Alzheimer's disease, with special emphasis on their role in modulating oxidative stress and inflammation and also examine their potential as therapeutic agents.

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