scholarly journals Effects of agmatine on chlorpromazine-induced neuronal injury in rat

2018 ◽  
Vol 87 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Bratislav Dejanovic ◽  
Vesna Vukovic-Dejanovic ◽  
Milica Ninkovic ◽  
Irena Lavrnja ◽  
Ivana Stojanovic ◽  
...  
Keyword(s):  
Nitrosative Stress ◽  
Combined Treatment ◽  
Brain Regions ◽  
Antioxidant Defence ◽  
Superoxide Anion Production ◽  
Beneficial Effects ◽  
Antioxidant Defence System ◽  
Oxide Concentration ◽  
Nitric Oxide Concentration ◽  
The Brain

This study was aimed to study the potentially beneficial effects of agmatine on oxidative/nitrosative stress development in the brain of Wistar rats during subacute chlorpromazine treatment. The animals were divided into control (0.9% saline), chlorpromazine (38.7 mg/kg b.w.), chlorpromazine+agmatine (agmatine 75 mg/kg b.w. immediately after chlorpromazine, 38.7 mg/kg b.w. i.p.) and agmatine (75 mg/kg b.w.) groups. All the tested substances were administered intraperitoneally for 15 consecutive days and the rats were sacrificed by decapitation on day 15. Subacute administration of chlorpromazine resulted in increased lipid peroxidation, nitric oxide concentration and superoxide anion production, while completely damaging the antioxidant defence system in the cerebral cortex, striatum, and hippocampus. However, the combined treatment with chlorpromazine and agmatine significantly attenuated the oxidative/nitrosative stress indices and restored the antioxidant capacity to the control values in all of the examined brain regions. Western blot analysis supported biochemical findings in all groups, but the most notable changes were found in the hippocampus. Our results suggest potentially beneficial effects of agmatine, which may be useful in the modified antioxidant approach in chlorpromazine-therapy.

scholarly journals Neural Underpinnings of Obesity: The Role of Oxidative Stress and Inflammation in the Brain

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1018
Author(s):  
Caitlyn A. Mullins ◽  
Ritchel B. Gannaban ◽  
Md Shahjalal Khan ◽  
Harsh Shah ◽  
Md Abu B. Siddik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Homeostasis ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Obesity Prevalence ◽  
Beneficial Effects ◽  
The Brain

Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.

Histopathological alterations in the brain regions of rats after perinatal combined treatment with cadmium and dexamethasone

Toxicology ◽  
2001 ◽  
Vol 161 (3) ◽  
pp. 189-199 ◽  
Author(s):  
M. Méndez-Armenta ◽  
R. Barroso-Moguel ◽  
J. Villeda-Hernández ◽  
C. Nava-Ruı́z ◽  
C. Rı́os
Keyword(s):  
Combined Treatment ◽  
Brain Regions ◽  
Histopathological Alterations ◽  
The Brain

scholarly journals Brain ACE2 overexpression reduces DOCA-salt hypertension independently of endoplasmic reticulum stress

2015 ◽  
Vol 308 (5) ◽  
pp. R370-R378 ◽  
Author(s):  
Huijing Xia ◽  
Thyago Moreira de Queiroz ◽  
Srinivas Sriramula ◽  
Yumei Feng ◽  
Tanya Johnson ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Fluorescent Protein ◽  
Brain Regions ◽  
Salt Treatment ◽  
Neurogenic Hypertension ◽  
Beneficial Effects ◽  
Salt Hypertension ◽  
The Impact ◽  
The Brain

Endoplasmic reticulum (ER) stress was previously reported to contribute to neurogenic hypertension while neuronal angiotensin-converting enzyme type 2 (ACE2) overexpression blunts the disease. To assess which brain regions are important for ACE2 beneficial effects and the contribution of ER stress to neurogenic hypertension, we first used transgenic mice harboring a floxed neuronal hACE2 transgene (SL) and tested the impact of hACE2 knockdown in the subfornical organ (SFO) and paraventricular nucleus (PVN) on deoxycorticosterone acetate (DOCA)-salt hypertension. SL and nontransgenic (NT) mice underwent DOCA-salt or sham treatment while infected with an adenoassociated virus (AAV) encoding Cre recombinase (AAV-Cre) or a control virus (AAV-green fluorescent protein) to the SFO or PVN. DOCA-salt-induced hypertension was reduced in SL mice, with hACE2 overexpression in the brain. This reduction was only partially blunted by knockdown of hACE2 in the SFO or PVN, suggesting that both regions are involved but not essential for ACE2 regulation of blood pressure (BP). DOCA-salt treatment did not increase the protein levels of ER stress and autophagy markers in NT mice, despite a significant increase in BP. In addition, these markers were not affected by hACE2 overexpression in the brain, despite a significant reduction of hypertension in SL mice. To further assess the role of ER stress in neurogenic hypertension, NT mice were infused intracerebroventricularlly with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor, during DOCA-salt treatment. However, TUDCA infusion failed to blunt the development of hypertension in NT mice. Our data suggest that brain ER stress does not contribute to DOCA-salt hypertension and that ACE2 blunts neurogenic hypertension independently of ER stress.

Antioxidant and bioenergetic coupling between neurons and astrocytes

2012 ◽  
Vol 443 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Seila Fernandez-Fernandez ◽  
Angeles Almeida ◽  
Juan P. Bolaños
Keyword(s):  
Nitrosative Stress ◽  
Pentose Phosphate ◽  
Therapeutic Interventions ◽  
Biochemical Mechanism ◽  
Intercellular Coupling ◽  
Antioxidant Defence ◽  
Oxidative And Nitrosative Stress ◽  
Novel Targets ◽  
The Brain ◽  
Reduced State

Oxidative and nitrosative stress underlie the pathogenesis of a broad range of human diseases, in particular neurodegenerative disorders. Within the brain, neurons are the cells most vulnerable to excess reactive oxygen and nitrogen species; their survival relies on the antioxidant protection promoted by neighbouring astrocytes. However, neurons are also intrinsically equipped with a biochemical mechanism that links glucose metabolism to antioxidant defence. Neurons actively metabolize glucose through the pentose phosphate pathway, which maintains the antioxidant glutathione in its reduced state, hence exerting neuroprotection. This process is tightly controlled by a key glycolysis-promoting enzyme and is dependent on an appropriate supply of energy substrates from astrocytes. Thus brain bioenergetic and antioxidant defence is coupled between neurons and astrocytes. A better understanding of the regulation of this intercellular coupling should be important for identifying novel targets for future therapeutic interventions.

Biochemical and electrocardiographic studies on the beneficial effects of gallic acid in cyclophosphamide-induced cardiorenal dysfunction

2017 ◽  
Vol 14 (3) ◽  
Author(s):  
Omolola Rachel Ogunsanwo ◽  
Ademola Adetokunbo Oyagbemi ◽  
Temidayo Olutayo Omobowale ◽  
Ebunoluwa Racheal Asenuga ◽  
Adebowale Bernard Saba
Keyword(s):  
Gallic Acid ◽  
Radical Scavenging Activity ◽  
Antineoplastic Agent ◽  
Radical Scavenging ◽  
Antioxidant Defence ◽  
Beneficial Effects ◽  
Progressive Heart Failure ◽  
Antioxidant Defence System ◽  
Life Threatening ◽  
Enzymic Antioxidants

AbstractBackgroundCardiac toxicity is one of the life-threatening complications of cancer therapy. Cyclophosphamide (CYP) is an alkylating agent with potent antineoplastic and immunosuppressive properties and possibly the most widely used antineoplastic agent. Chronic cardiotoxicity associated with CYP is characterized by progressive heart failure developing from weeks to years after therapy.MethodsIn this study, rats were administered with (60 mg/kg and 120 mg/kg) alone or in combination with single intraperitoneal (200 mg/kg) administration of CYP for 7 days. CYP was only administered on day 1.ResultsThe administration of CYP led to a significant (p<0.05) increase in cardiac and renal malondialdehyde (MDA) contents and hydrogen peroxide (HConclusionsIn this study, treatment with gallic acid (60 mg/kg and 120 mg/kg) restored the enzymic and non-enzymic antioxidants and also attenuated cardiotoxic and nephrotoxic effect of CYP through free radical scavenging activity, anti-inflammatory and improvement of antioxidant defence system.

A dynamic mouse peptidome landscape reveals probiotic modulation of the gut-brain axis

2020 ◽  
Vol 13 (642) ◽  
pp. eabb0443 ◽  
Author(s):  
Pei Zhang ◽  
Xiaoli Wu ◽  
Shan Liang ◽  
Xianfeng Shao ◽  
Qianqian Wang ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Brain Regions ◽  
Literature Mining ◽  
Functional Roles ◽  
Beneficial Effects ◽  
Probiotic Treatment ◽  
Dynamic Landscape ◽  
The Central Nervous System ◽  
The Brain

Certain probiotics have beneficial effects on the function of the central nervous system through modulation of the gut-brain axis. Here, we describe a dynamic landscape of the peptidome across multiple brain regions, modulated by oral administration of different probiotic species over various times. The spatiotemporal and strain-specific changes of the brain peptidome correlated with the composition of the gut microbiome. The hippocampus exhibited the most sensitive response to probiotic treatment. The administration of heat-killed probiotics altered the hippocampus peptidome but did not substantially change the gut microbiome. We developed a literature-mining algorithm to link the neuropeptides altered by probiotics with potential functional roles. We validated the probiotic-regulated role of corticotropin-releasing hormone by monitoring the hypothalamic-pituitary-adrenal axis, the prenatal stress–induced hyperactivity of which was attenuated by probiotics treatment. Our findings provide evidence for modulation of the brain peptidome by probiotics and provide a resource for further studies of the gut-brain axis and probiotic therapies.

Therapeutic Approaches to Alzheimer’s Type of Dementia: A Focus on FGF21 Mediated Neuroprotection

2019 ◽  
Vol 25 (23) ◽  
pp. 2555-2568 ◽  
Author(s):  
Rajeev Taliyan ◽  
Sarathlal K. Chandran ◽  
Violina Kakoty
Keyword(s):  
Diabetes Mellitus ◽  
Protein Trafficking ◽  
Metabolic Stress ◽  
Insulin Receptors ◽  
Metabolic Dysfunction ◽  
Beneficial Effects ◽  
Glucose And Lipid Metabolism ◽  
Endocrine Hormone ◽  
Metabolic Conditions ◽  
The Brain

Neurodegenerative disorders are the most devastating disorder of the nervous system. The pathological basis of neurodegeneration is linked with dysfunctional protein trafficking, mitochondrial stress, environmental factors and aging. With the identification of insulin and insulin receptors in some parts of the brain, it has become evident that certain metabolic conditions associated with insulin dysfunction like Type 2 diabetes mellitus (T2DM), dyslipidemia, obesity etc., are also known to contribute to neurodegeneration mainly Alzheimer’s Disease (AD). Recently, a member of the fibroblast growth factor (FGF) superfamily, FGF21 has proved tremendous efficacy in diseases like diabetes mellitus, obesity and insulin resistance (IR). Increased levels of FGF21 have been reported to exert multiple beneficial effects in metabolic syndrome. FGF21 receptors are present in certain areas of the brain involved in learning and memory. However, despite extensive research, its function as a neuroprotectant in AD remains elusive. FGF21 is a circulating endocrine hormone which is mainly secreted by the liver primarily in fasting conditions. FGF21 exerts its effects after binding to FGFR1 and co-receptor, β-klotho (KLB). It is involved in regulating energy via glucose and lipid metabolism. It is believed that aberrant FGF21 signalling might account for various anomalies like neurodegeneration, cancer, metabolic dysfunction etc. Hence, this review will majorly focus on FGF21 role as a neuroprotectant and potential metabolic regulator. Moreover, we will also review its potential as an emerging candidate for combating metabolic stress induced neurodegenerative abnormalities.

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