scholarly journals Curcumin Ameliorates the Cd-Induced Anxiety-like Behavior in Mice by Regulating Oxidative Stress and Neuro-Inflammatory Proteins in the Prefrontal Cortex Region of the Brain

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1710
Author(s):  
Dhondup Namgyal ◽  
Sher Ali ◽  
Muhammad Delwar Hussain ◽  
Mohsin Kazi ◽  
Ajaz Ahmad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Working Memory ◽  
Prefrontal Cortex ◽  
Neurodegenerative Diseases ◽  
Spatial Working Memory ◽  
Cellular Mechanisms ◽  
Behavioral Impairment ◽  
Age Related ◽  
The Brain ◽  
And Oxidative Stress

Age-related neurodegenerative diseases and vascular dementia are major challenges to the modern health care system. Most neurodegenerative diseases are associated with impaired spatial working memory and anxiety-like behavior. Thus, it is important to understand the underlying cellular mechanisms of neurodegenerative diseases in different regions of the brain to develop an effective therapeutic approach. In our previous research paper, we have reported the ameliorative effect of curcumin in Cd-induced hippocampal neurodegeneration. However, recently many researchers had reported the important role of the prefrontal cortex in higher cognitive functions. Therefore, to look into the cellular mechanism of curcumin protection against Cd-induced prefrontal cortex neurotoxicity, we investigated spatial working memory, anxiety-like behavior and analyzed prefrontal cortex inflammatory markers (IL-6, IL-10, and TNFα), antioxidant enzymes (SOD, GSH, and CAT), and pro-oxidant MDA level. Further, we conducted histological studies of the prefrontal cortex in Swiss albino mice exposed to cadmium (2.5 mg/kg). We observed that curcumin treatment improved the spatial working memory and anxiety-like behavior of mice through reduction of prefrontal cortex neuroinflammation and oxidative stress as well as increasing the number of viable prefrontal cortex neuronal cells. Our result suggests that environmental heavy metal cadmium can induce behavioral impairment in mice through prefrontal cortex cellular inflammation and oxidative stress. We found that curcumin has a potential therapeutic property to mitigate these behavioral and biochemical impairments induced by cadmium.

scholarly journals Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020 ◽  
Vol 21 (7) ◽  
pp. 2501 ◽  
Author(s):  
Thomas Nury ◽  
Gérard Lizard ◽  
Anne Vejux
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Death ◽  
Neurodegenerative Diseases ◽  
The Body ◽  
Protein Accumulation ◽  
Common Features ◽  
Apoptosis And Inflammation ◽  
The Brain ◽  
And Oxidative Stress

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxicity induced during the pathology, whether at the level of mitochondria, oxidative stress or apoptosis and inflammation. The conclusions of the various studies cited are oriented towards the preventive use of oils or fatty acids. The future of these lipids that can be used in therapy/prevention will undoubtedly involve a better delivery to the body and to the brain by utilizing lipid encapsulation.

Protective effect of curcumin on diazepam-induced behavioral changes and oxidative stress in rats

2016 ◽  
Vol 33 (S1) ◽  
pp. s286-s286
Author(s):  
A. Sevastre-Berghian ◽  
V. Făgărăşăn ◽  
N. Decea ◽  
R. Moldovan ◽  
B. Sevastre ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Working Memory ◽  
Cognitive Performance ◽  
Spatial Working Memory ◽  
Vehicle Group ◽  
Behavioral Tests ◽  
Ambulatory Activity ◽  
Group I ◽  
Y Maze ◽  
And Oxidative Stress

IntroductionCurcumin (CUR), a polyphenolic compound, extracted from Curcuma longa, is known for its neuroprotective, antioxidant and anti-inflammatory effects.ObjectivesTo evaluate the effect of CUR on ambulatory activity, spatial working memory and on oxidative stress in rats induced by Diazepam (DZP) administration.AimsTo analyze whether CUR may improve the cognitive performance and offer systemic protection from oxidative stress.MethodsThe effect of CUR on DZP-induced memory impairment and oxidative stress was studied on Wistar rats. Group I received a vehicle, group II – vehicle and CUR, group III – vehicle and DZP, group IV – vehicle, CUR and DZP. CUR (150 mg/kg bw) and vehicle were orally administered for five weeks long. DZP (2 mg/kg bw) was administered i.p. 20 minutes before the behavioral tests. Behavioral tests, i.e. Open Field and Y Maze Test, were performed. Malondialdehyde and reduced glutathione/oxidized glutathione ratio were determined in the serum and brain tissue homogenate. Hippocampal sections were histologically assessed. The data were statistically analyzed by one-way ANOVA, followed by Dunns post-test.ResultsDZP decreased (P < 0.01) the number of spontaneous alternations, as compared to control group, thus suggesting an impairment of spatial working memory. Behavioral tests revealed no enhancing effect of CUR on spontaneous alternation behaviors in Y Maze. CUR reversed (P < 0.01) the inhibitory effect of diazepam (P < 0.05) on the ambulatory activity in OFT and decreased the lipid peroxidation in the serum (P < 0.05).ConclusionsThe results show that CUR may offer systemic protection from oxidative stress, thus improving the cognitive performance.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Impairment of spatial working memory and oxidative stress induced by repeated crack cocaine inhalation in rats

2019 ◽  
Vol 359 ◽  
pp. 910-917 ◽  
Author(s):  
Ingryd Fortes Souza Lipaus ◽  
Elisa Fraga Gomes ◽  
Cleciane Waldetário Martins ◽  
Cristina Martins e Silva ◽  
Rita Gomes Wanderley Pires ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Working Memory ◽  
Crack Cocaine ◽  
Spatial Working Memory ◽  
And Oxidative Stress

scholarly journals Serine Deficiency Exacerbates Inflammation and Oxidative Stress via Microbiota-Gut-Brain Axis in D-Galactose-Induced Aging Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Fengen Wang ◽  
Hongbin Zhou ◽  
Ligang Deng ◽  
Lei Wang ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Short Chain Fatty Acid ◽  
Inflammatory Responses ◽  
Basal Diet ◽  
Fecal Microbiota ◽  
Defense System ◽  
Age Related ◽  
The Brain ◽  
And Oxidative Stress ◽  
Microbiota Diversity

Inflammation and oxidative stress play key roles in the process of aging and age-related diseases. Since serine availability plays important roles in the support of antioxidant and anti-inflammatory defense system, we explored whether serine deficiency affects inflammatory and oxidative status in D-galactose-induced aging mice. Male mice were randomly assigned into four groups: mice fed a basal diet, mice fed a serine- and glycine-deficient (SGD) diet, mice injected with D-galactose and fed a basal diet, and mice injected with D-galactose and fed an SGD diet. The results showed that D-galactose resulted in oxidative and inflammatory responses, while serine deficiency alone showed no such effects. However, serine deficiency significantly exacerbated oxidative stress and inflammation in D-galactose-treated mice. The composition of fecal microbiota was affected by D-galactose injection, which was characterized by decreased microbiota diversity and downregulated ratio of Firmicutes/Bacteroidetes, as well as decreased proportion of Clostridium XIVa. Furthermore, serine deficiency exacerbated these changes. Additionally, serine deficiency in combination with D-galactose injection significantly decreased fecal butyric acid content and gene expression of short-chain fatty acid transporters (Slc16a3 and Slc16a7) and receptor (Gpr109a) in the brain. Finally, serine deficiency exacerbated the decrease of expression of phosphorylated AMPK and the increase of expression of phosphorylated NFκB p65, which were caused by D-galactose injection. In conclusion, our results suggested that serine deficiency exacerbated inflammation and oxidative stress in D-galactose-induced aging mice. The involved mechanisms might be partially attributed to the changes in the microbiota-gut-brain axis affected by serine deficiency.

scholarly journals When It Comes to an End: Oxidative Stress Crosstalk with Protein Aggregation and Neuroinflammation Induce Neurodegeneration

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 740 ◽  
Author(s):  
Patrycja Michalska ◽  
Rafael León
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Energy Demand ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
High Energy ◽  
Antioxidant Defenses ◽  
Loss Of Function ◽  
Age Related ◽  
The Brain

Neurodegenerative diseases are characterized by a progressive loss of neurons in the brain or spinal cord that leads to a loss of function of the affected areas. The lack of effective treatments and the ever-increasing life expectancy is raising the number of individuals affected, having a tremendous social and economic impact. The brain is particularly vulnerable to oxidative damage given the high energy demand, low levels of antioxidant defenses, and high levels of metal ions. Driven by age-related changes, neurodegeneration is characterized by increased oxidative stress leading to irreversible neuronal damage, followed by cell death. Nevertheless, neurodegenerative diseases are known as complex pathologies where several mechanisms drive neuronal death. Herein we discuss the interplay among oxidative stress, proteinopathy, and neuroinflammation at the early stages of neurodegenerative diseases. Finally, we discuss the use of the Nrf2-ARE pathway as a potential therapeutic strategy based on these molecular mechanisms to develop transformative medicines.

scholarly journals Interplay between MicroRNAs and Oxidative Stress in Neurodegenerative Diseases

2019 ◽  
Vol 20 (23) ◽  
pp. 6055 ◽  
Author(s):  
Konovalova ◽  
Gerasymchuk ◽  
Parkkinen ◽  
Chmielarz ◽  
Domanskyi
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Regulatory Networks ◽  
Neuroprotective Activity ◽  
Microrna Regulation ◽  
Cellular Models ◽  
Age Related ◽  
Microrna Networks ◽  
And Oxidative Stress

MicroRNAs are post-transcriptional regulators of gene expression, crucial for neuronal differentiation, survival, and activity. Age-related dysregulation of microRNA biogenesis increases neuronal vulnerability to cellular stress and may contribute to the development and progression of neurodegenerative diseases. All major neurodegenerative disorders are also associated with oxidative stress, which is widely recognized as a potential target for protective therapies. Albeit often considered separately, microRNA networks and oxidative stress are inextricably entwined in neurodegenerative processes. Oxidative stress affects expression levels of multiple microRNAs and, conversely, microRNAs regulate many genes involved in an oxidative stress response. Both oxidative stress and microRNA regulatory networks also influence other processes linked to neurodegeneration, such as mitochondrial dysfunction, deregulation of proteostasis, and increased neuroinflammation, which ultimately lead to neuronal death. Modulating the levels of a relatively small number of microRNAs may therefore alleviate pathological oxidative damage and have neuroprotective activity. Here, we review the role of individual microRNAs in oxidative stress and related pathways in four neurodegenerative conditions: Alzheimer’s (AD), Parkinson’s (PD), Huntington’s (HD) disease, and amyotrophic lateral sclerosis (ALS). We also discuss the problems associated with the use of oversimplified cellular models and highlight perspectives of studying microRNA regulation and oxidative stress in human stem cell-derived neurons.

scholarly journals Trying to Put the Puzzle Together: Age and Performance Level Modulate the Neural Response to Increasing Task Load within Left Rostral Prefrontal Cortex

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Eva Bauer ◽  
Gebhard Sammer ◽  
Max Toepper
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Spatial Working Memory ◽  
Load Level ◽  
Performance Level ◽  
Significant Group ◽  
Task Load ◽  
Age Related ◽  
And Performance ◽  
Rostral Prefrontal Cortex

Age-related working memory decline is associated with functional cerebral changes within prefrontal cortex (PFC). Kind and meaning of these changes are heavily discussed since they depend on performance level and task load. Hence, we investigated the effects of age, performance level, and load on spatial working memory retrieval-related brain activation in different subregions of the PFC. 19 younger (Y) and 21 older (O) adults who were further subdivided into high performers (HP) and low performers (LP) performed a modified version of the Corsi Block-Tapping test during fMRI. Brain data was analyzed by a 4 (groups: YHP, OHP, YLP, and OLP) × 3 (load levels: loads 4, 5, and 6) ANOVA. Results revealed significant group × load interaction effects within rostral dorsolateral and ventrolateral PFC. YHP showed a flexible neural upregulation with increasing load, whereas YLP reached a resource ceiling at a moderate load level. OHP showed a similar (though less intense) pattern as YHP and may have compensated age-effects at high task load. OLP showed neural inefficiency at low and no upregulation at higher load. Our findings highlight the relevance of age and performance level for load-dependent activation within rostral PFC. Results are discussed in the context of the compensation-related utilization of neural circuits hypothesis (CRUNCH) and functional PFC organization.

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