Behavior and oxidative stress parameters in rats subjected to the animal's models induced by chronic mild stress and 6-hydroxydopamine

Tuon, Talita; Meirelles, Sandra S.; Moura, Airam B. de; Rosa, Thayse; Borba, Laura A.; Botelho, Maria Eduarda M.; Abelaira, Helena M.; Mathia, Gisiane B.; Danielski, Lucinéia Gainski; Fileti, Maria Eduarda; Petronilho, Fabrícia; Ignácio, Zuleide Maria; Quevedo, Joao L De; Réus, Gislaine Z.

doi:10.1016/j.bbr.2021.113226

Cited by 12 publications

(7 citation statements)

References 89 publications

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“…The earlier studies showed that the administration of rotenone increases ROS generation and oxidative stress by reducing GSH, catalase, and SOD concentration and improving MDA and nitrite concentration in rats. 35,36 Similarly, the current study observed that rotenone declined antioxidant levels and increased MDA and nitrite levels in the striatum. Moreover, pretreatment of the BCG vaccine significantly attenuated the rise in MDA and nitrite concentration and restored the GSH, SOD, and catalase concentration, indicating an antioxidant potential.…”

Section: Discussionsupporting

confidence: 77%

Effect of Bacille‐Calmette‐Guerin vaccine against rotenone‐induced Parkinson's disease: Role of neuroinflammation and neurotransmitters

Yedke,

Soni,

Kumar

2023

Fundamemntal Clinical Pharma

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BackgroundParkinson's disease (PD) is an extrapyramidal movement disorder associated with a hypokinetic condition generated by impairment in dopaminergic neuronal viability in the nigrostriatal region of the brain. Current medications can only provide symptomatic management; to date, no permanent cure is available. To compensate for this lacuna, researchers are gaining interest in antigen‐based therapy, and Bacille‐Calmette‐Guerin (BCG) is one of the vaccines with a high safety margin that acts by stimulating immunoreactive T‐cells in the CNS and reducing expression of pro‐inflammatory cytokines including interleukin (IL)‐1β and tumor necrotic factor (TNF‐α) to produce neuroprotection. A previous study reported that BCG exerts a neuroprotective effect against several neurodegenerative disorders, such as Alzheimer's disease.ObjectiveThe objective of this study is to explore the neuroprotective effect of the BCG vaccine against the rotenone model of PD.MethodsRotenone (1.5 mg/kg, s.c) for 28 days, and BCG vaccine (2 × 107 cfu, i.p) single dose was injected to rats, and behavioral assessments were performed on the 21st and 28th day. On the 29th day, rats were sacrificed, and brains were isolated for biochemical and neurochemical estimation.ResultsBCG vaccine significantly restored rotenone‐induced motor deficits (open field test, narrow beam walk, and rotarod), biochemical levels (GSH, SOD, catalase, MDA, and nitrite), neurotransmitters (dopamine, 5‐hydroxy tryptamine, norepinephrine, 3,4‐dihydroxyphenylacetic acid, hemovanillic acid, and 5‐hydroxy indoleacetic acid), and levels of inflammatory cytokines (IL‐1β and TNF‐α) in the striatum. It also prevents histopathological changes by reducing eosinophilic lesions in the striatum.ConclusionFrom the results, we conclude that BCG vaccine showed neuroprotection through antioxidant and anti‐inflammatory effect. Thus, in the future, it can be used as a neuroprotective agent for other neurological disorders, including PD.

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Section: Discussionsupporting

confidence: 77%

Effect of Bacille‐Calmette‐Guerin vaccine against rotenone‐induced Parkinson's disease: Role of neuroinflammation and neurotransmitters

Yedke,

Soni,

Kumar

2023

Fundamemntal Clinical Pharma

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“…Impairment of cognitive flexibility is mainly associated with the monoamine system of the PFC [ 82 ]. Oxidative stress is also a crucial way of stress to affect the PFC [ 55 , 83 ]. As depression often cooccurs with cognitive impairment, the PFC is considered an important brain region in depression [ 82 ].…”

Section: Neurological Links Between Stress and Key Brain Regionsmentioning

confidence: 99%

Section: Neurological Links Between Stress and Key Brain Regionsmentioning

confidence: 99%

“…Moreover, after stress, rats exhibited a significant increase of the content of protein carbonyl, total glutathione (GSH) [ 55 , 83 ], and malondialdehyde (MDA) level and a decrease of SOD activity or BDNF level in PFC [ 50 , 83 , 93 ]. Oxidative stress induced by chronic stress can lead to mPFC damage and decreased hippocampal neurogenesis [ 94 ], eventually leading to depression [ 47 , 51 , 55 , 83 , 93 , 94 ] or anxiety-like behavior [ 27 , 50 ]. CUMS exposure also significantly decreased GSH, BDNF, phosphorylation of AKT, and mTOR in PFC [ 50 , 51 , 93 ], and antioxidant drugs such as resveratrol [ 93 ], 5-HT [ 95 ], or carvedilol [ 96 ] can increase BDNF, AKT, and mTOR and decrease oxidative stress, significantly alleviating depression.…”

Section: Neurological Links Between Stress and Key Brain Regionsmentioning

confidence: 99%

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Neurobiological Links between Stress, Brain Injury, and Disease

Guo

Zheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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Stress, which refers to a combination of physiological, neuroendocrine, behavioral, and emotional responses to novel or threatening stimuli, is essentially a defensive adaptation under physiological conditions. However, strong and long-lasting stress can lead to psychological and pathological damage. Growing evidence suggests that patients suffering from mild and moderate brain injuries and diseases often show severe neurological dysfunction and experience severe and persistent stressful events or environmental stimuli, whether in the acute, subacute, or recovery stage. Previous studies have shown that stress has a remarkable influence on key brain regions and brain diseases. The mechanisms through which stress affects the brain are diverse, including activation of endoplasmic reticulum stress (ERS), apoptosis, oxidative stress, and excitatory/inhibitory neuron imbalance, and may lead to behavioral and cognitive deficits. The impact of stress on brain diseases is complex and involves impediment of recovery, aggravation of cognitive impairment, and neurodegeneration. This review summarizes various stress models and their applications and then discusses the effects and mechanisms of stress on key brain regions—including the hippocampus, hypothalamus, amygdala, and prefrontal cortex—and in brain injuries and diseases—including Alzheimer’s disease, stroke, traumatic brain injury, and epilepsy. Lastly, this review highlights psychological interventions and potential therapeutic targets for patients with brain injuries and diseases who experience severe and persistent stressful events.

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“…To date, much progress has been made in the study of the potential etiology of depression, such as the involvement of monoamine neurotransmitters (serotonin, norepinephrine and dopamine) [ 4 ], brain-derived neurotrophic factor (BDNF) [ 5 ], hypothalamic-pituitary-adrenal (HPA) axis [ 6 ], corticotrophin releasing hormone (CRH) [ 7 ], chronic systemic inflammation [ 8 ], glutamate metabolism [ 9 ], neuronal synaptic plasticity [ 10 ] and oxidative stress [ 11 ] et al Research showed that serotonin deficiency may lead to the incidence of depression [ 12 ], which is currently one of the generally accepted hypotheses. The decrease of norepinephrine and dopamine in the blood and cerebrospinal fluid of patients with depression suggests a relationship between depression and monoamine neurotransmitters [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Potential biomarkers: differentially expressed proteins of the extrinsic coagulation pathway in plasma samples from patients with depression

Zhang

Shi

et al. 2021

Bioengineered

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Depression is a severe disabling psychiatric illness and the pathophysiological mechanisms remain unknown. In previous work, we found the changes in extrinsic coagulation (EC) pathway proteins in depressed patients compared with healthy subjects were significant. In this study, we screened differentially expressed proteins (DEPs) in the EC pathway, and explored the molecular mechanism by constructing a protein-protein interaction (PPI) network. The DEPs of the EC pathwaywere initially screened by isobaric tags for relative and absolute quantification (iTRAQ) in plasma samples obtained from 20 depression patients and 20 healthy controls, and were then identified by Enzyme-linked immunosorbent assays (ELISAs). Ingenuity Pathway Analysis (IPA) software was used to analyse pathway. The differentially expressed genes (DEGs) were identified by analyzing the GSE98793 microarray data from the Gene Expression Omnibus database using the Significance Analysis for Microarrays (SAM, version 4.1) statistical method. Cytoscape version 3.4.0 software was used to construct and visualize PPI networks. The results show that Fibrinogen alpha chain (FGA), Fibrinogen beta chain (FGB), Fibrinogen gamma chain (FGG) and Coagulation factor VII (FVII) were screened in the EC pathway from depression patient samples. FGA, FGB, and FGG were significantly up-regulated, and FVII was down-regulated. Thirteen DEGs related to depression and EC pathways were identified from the microarray database. Among them NF-κB Inhibitor Beta (NFKBIB) and Heat shock protein family B (small) member 1 (HSPB1) were highly correlated with EC pathway. We conclude that EC pathway is associated with depression, which provided clues for the biomarker development and the pathogenesis of depression.

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Behavior and oxidative stress parameters in rats subjected to the animal's models induced by chronic mild stress and 6-hydroxydopamine

Cited by 12 publications

References 89 publications

Effect of Bacille‐Calmette‐Guerin vaccine against rotenone‐induced Parkinson's disease: Role of neuroinflammation and neurotransmitters

Effect of Bacille‐Calmette‐Guerin vaccine against rotenone‐induced Parkinson's disease: Role of neuroinflammation and neurotransmitters

Neurobiological Links between Stress, Brain Injury, and Disease

Potential biomarkers: differentially expressed proteins of the extrinsic coagulation pathway in plasma samples from patients with depression

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