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.

scholarly journals NEUROPROTECTIVE EFFECT OF WATERMELON (CITRULLUS LANATUS) PULP JUICE ON SCOPOLAMINE-INDUCED MEMORY DEFICITS IN SWISS ALBINO MICE: THE ROLE OF ACETYLCHOLINESTERASE AND OXIDATIVE STRESS

2021 ◽  
Vol 12 (3) ◽  
pp. 52-56
Author(s):  
Divya N ◽  
Amudha P ◽  
Viveka K Priya
Keyword(s):  
Oxidative Stress ◽  
Ache Activity ◽  
Citrullus Lanatus ◽  
Neuroprotective Effect ◽  
Memory Deficits ◽  
Memory Deficit ◽  
Stress Indicators ◽  
Oxidative Stress Indicators ◽  
And Oxidative Stress

The effect of Watermelon (Citrullus lanatus) Pulp Juice (WPJ) on scopolamine (SCOP) induced memory deficits is due to the involvement of oxidative stress and AChE activity. The juice was obtained by crushing the pulp in blender and three different concentrations of 100%, 50% and 25% was administration to prevent memory deficit by evaluating changes of AChE activity and oxidative stress indicators (SOD, CAT, LPO and GPx) induced by scopolamine. These results provide evidence that WPJ is an alternative to protect SCOP induced memory deficits in mice by involvement of oxidative stress and AChE activity.

Melatonin reverses H-89 induced spatial memory deficit: Involvement of oxidative stress and mitochondrial function

2017 ◽  
Vol 316 ◽  
pp. 115-124 ◽  
Author(s):  
Rojin Sharif ◽  
Mehdi Aghsami ◽  
Mehdi Gharghabi ◽  
Mehdi Sanati ◽  
Tina Khorshidahmad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spatial Memory ◽  
Mitochondrial Function ◽  
Memory Deficit ◽  
Spatial Memory Deficit

Astaxanthin ameliorates scopolamine-induced spatial memory deficit via reduced cortical-striato-hippocampal oxidative stress

2019 ◽  
Vol 1710 ◽  
pp. 74-81 ◽  
Author(s):  
Md. Mamun Al-Amin ◽  
Waich Mahmud ◽  
Mst. Shahnaj Pervin ◽  
S.M. Ridwanul Islam ◽  
Muhammad Ashikur Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spatial Memory ◽  
Memory Deficit ◽  
Spatial Memory Deficit

scholarly journals Diaportheone A Analogues Instigate a Neuroprotective Effect by Protecting Neuroblastoma SH-SY5Y Cells from Oxidative Stress

Biology ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 199
Author(s):  
Mario A. Tan ◽  
Elena Zakharova ◽  
Seong Soo A. An
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Membrane ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Stress Effects ◽  
Intracellular Ros ◽  
Aβ Aggregation ◽  
Protein Models ◽  
First Time

Alzheimer’s disease (AD) remains an incurable neurodegenerative illness. Oxidative stress resulting in the formation of reactive oxygen species (ROS) and the abnormal deposition of amyloid-beta (Aβ) are the major pathological hallmarks associated with AD. In search for small molecules targeting multiple pathways of AD and of no known molecular targets, the neuroprotective effects of the synthetic chromones diaportheone A1 and diaportheone A2, analogues of the natural product diaportheone A, were investigated. Chromones are heterocyclic compounds bearing the benzoannelated γ-pyrone moiety and were regarded as an important class of organic molecules due to their diverse pharmacological activities. The influence of the compounds on the inhibition of Aβ aggregation was determined by Thioflavin T (ThT) assay, and the cell viability, ROS, and mitochondrial membrane potential were evaluated with human neuroblastoma SH-SY5Y cells. Results showed that both compounds inhibited the Aβ aggregation at 80.41% and 73.68% for diaportheone A1 and diaportheone A2, respectively. Increased cell viabilities were observed from the protection by both compounds using Aβ- or H2O2-induced SH-SY5Y cells. Both compounds also reduced the intracellular ROS level in Aβ- or H2O2-induced SH-SY5Y cells at 10 and 20 μM concentrations, and increased the mitochondrial membrane potentials in Aβ-induced SH-SY5Y cells at 20 μM concentration. Molecular docking experiments using the Aβ protein models 2MXU and 2BEG also indicated a good agreement with the experimental data. The results demonstrated for the first time the oxidative stress effects associated with the chromones diaportheone A1 and diaportheone A2 as potential neuroprotective therapeutic agents against AD.

scholarly journals Neuroprotective Effect of Gallic Acid on Memory Deficit and Content of BDNF in Brain Entorhinal Cortex of Rat’s Offspring in Uteroplacental Insufficiency Model

2020 ◽  
Author(s):  
Zahra Esfandiari ◽  
Mohammad Amin Edalatmanesh
Keyword(s):  
Gallic Acid ◽  
Entorhinal Cortex ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Memory Deficit ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Y Maze ◽  
Spss Software ◽  
Post Hoc

Introduction: Uteroplacental insufficiency (UPI) causes neurodevelopmental deficits affecting the intrauterine growth restricted (IUGR) offspring. This study aimed to analyze the effects of Gallic acid (GA) on memory deficit and brain-derived neurotrophic factor (BDNF) content in entorhinal cortex of UPI rat models. Methods: In this experimental study, 40 pregnant Wistar rats were randomly divided into 5 groups, including: control, UPI, UPI+GA100, UPI+GA200and UPI+GA400. For IUGR induction, anterior uterine artery occlusion surgery was carried out on gestation day (GD) 18. From GD15, GA was administrated orally, in 100, 200 and 400 mg/kg BW doses until the birth of their neonates. Spatial and working memories are analyzed by Morris water maze and Y maze at postnatal day (PND) 30, respectively. Then, BDNF cerebral cortex level was estimated using ELISA technique.The data were analyzed through ANOVA and Tukey Post hoc in SPSS software version 16. Results: A significant decrease was observed in spatial and working memories and BDNF content in entorhinal cortex of UPI group in comparison with the control group (p˂0.05). On the other hand, GA-treated groups showed a significant increase in BDNF content and amelioration of spatial and working memories (p˂0.05). Conclusion: Fetal growth restrictionafter UPI by decreasingBDNFlevel in entorhinal cortex caused memory deficits in rat’s model. Moreover, neuroprotective effects of GA lead to increased BDNF content and ameliorate cognitive deficits in UPI model.

scholarly journals Differential effects of alkaloids on memory in rodents

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Patrick M. Callahan ◽  
Alvin V. Terry ◽  
Manuel C. Peitsch ◽  
Julia Hoeng ◽  
Kyoko Koshibu
Keyword(s):  
Spatial Memory ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Memory Function ◽  
Critical Role ◽  
Memory Deficit ◽  
Short Term ◽  
General Role ◽  
Y Maze ◽  
Spatial Memory Deficit

AbstractNicotinic acetylcholine receptors (nAChRs) play a critical role in the neuropharmacology of learning and memory. As such, naturally occurring alkaloids that regulate nAChR activity have gained interest for understanding and potentially improving memory function. In this study, we tested the acute effects of three known nicotinic alkaloids, nicotine, cotinine, and anatabine, in suppressing scopolamine-induced memory deficit in rodents by using two classic memory paradigms, Y-maze and novel object recognition (NOR) in mice and rats, respectively. We found that all compounds were able to suppress scopolamine-induced spatial memory deficit in the Y-maze spontaneous alternation paradigm. However, only nicotine was able to suppress the short-term object memory deficit in NOR, despite the higher doses of cotinine and anatabine used to account for their potential differences in nAChR activity. These results indicate that cotinine and anatabine can uniquely regulate short-term spatial memory, while nicotine seems to have more robust and general role in memory regulation in rodents. Thus, nAChR-activating alkaloids may possess distinct procognitive properties in rodents, depending on the memory types examined.

scholarly journals A Novel Peroxidase Mimics and Ameliorates Alzheimer’s Disease-Related Pathology and Cognitive Decline in Mice

2018 ◽  
Vol 19 (11) ◽  
pp. 3304 ◽  
Author(s):  
Jia Xu ◽  
Kai Wang ◽  
Ye Yuan ◽  
Hui Li ◽  
Ruining Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Decline ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Learning Ability ◽  
Human Neuroblastoma ◽  
Peroxidase Mimics

Alzheimer’s disease (AD) is the most common neurodegenerative disorder in the elderly, which is characterized by the accumulation of amyloid β (Aβ) plaques, oxidative stress, and neuronal loss. Therefore, clearing Aβ aggregates and reducing oxidative stress could be an effective therapeutic strategy for AD. Deuterohemin-AlaHisThrValGluLys (DhHP-6), a novel deuterohemin-containing peptide mimetic of the natural microperoxidase-11 (MP-11), shows higher antioxidant activity and stability compared to the natural microperoxidases. DhHP-6 possesses the ability of extending lifespan and alleviating paralysis in the Aβ1-42 transgenic Caenorhabditis elegans CL4176 model of AD, as shown in our previous study. Therefore, this study was aimed at exploring the neuroprotective effect of DhHP-6 in the APPswe/PSEN1dE9 transgenic mouse model of AD. DhHP-6 reduced the diameter and fiber structure of Aβ1-42 aggregation in vitro, as shown by dynamic light scattering and transmission electron microscope. DhHP-6 exerted its neuroprotective effect by inhibiting Aβ aggregation and plaque formation, and by reducing Aβ1-42 oligomers-induced neurotoxicity on HT22 (mouse hippocampal neuronal) and SH-SY5Y (human neuroblastoma) cells. In the AD mouse model, DhHP-6 significantly ameliorated cognitive decline and improved spatial learning ability in behavioral tests including the Morris water maze, Y-maze, novel object recognition, open field, and nest-building test. Moreover, DhHP-6 reduced the deposition of Aβ plaques in the cerebral cortex and hippocampus. More importantly, DhHP-6 restored the morphology of astrocytes and microglia, and significantly reduced the levels of pro-inflammatory cytokines. Our findings provide a basis for considering the non-toxic, peroxidase mimetic DhHP-6 as a new candidate drug against AD.

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.

Sign in / Sign up

Export Citation Format

Share Document