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Nanotechnology as a therapeutic strategy to prevent neuropsychomotor alterations associated with hypercholesterolemia

Hypercholesterolemia has been linked to neurodegenerative disease development. Previously others and we demonstrated that high levels of plasma cholesterol-induced memory impairments and depressive-like behavior in mice. More recently, some evidence reported that a hypercholesterolemic diet led to motor alterations in rodents. Peripheral inflammation, blood-brain barrier (BBB) dysfunction, and neu

Subcellular localization of sphingosine 1-phosphate receptors in synapses of the mouse cortex

Sphingosine 1-phosphate (S1P) has pleiotropic biological functions in the regulation of proliferation, survival, migration, inflammation or angiogenesis. S1P acts as intracellular second messenger, as well as extracellular receptor ligand via five G-protein coupled receptors (S1PR1-5). In the brain, S1P regulates neuronal proliferation or apoptosis, excitatory neurotransmission and neuroglia activ

Exploratory Data Analysis of Cell and Mitochondrial High-Fat, High-Sugar Toxicity on Human HepG2 Cells

Non-alcoholic steatohepatitis (NASH), one of the deleterious stages of non-alcoholic fatty liver disease, remains a significant cause of liver-related morbidity and mortality worldwide. In the current work, we used an exploratory data analysis to investigate time-dependent cellular and mitochondrial effects of different supra-physiological fatty acids (FA) overload strategies, in the presence or a

Afrostyrax lepidophyllus Mildbr. and Monodora myristica (Gaertn.) Dunal Extracts Decrease Doxorubicin Cytotoxicity on H9c2 Cardiomyoblasts

Materials and Methods: Bark extracts of these plants (1 and 25 µg/mL) were added 3 hours before coincubating H9c2 cardiomyoblasts with Dox (0.5 and 1 µM) for 24 hours more. We measured cell mass and metabolic viability, mitochondrial transmembrane potential, superoxide anion content, and activity-like of caspase-3 and caspase-9 following treatment with the extracts and/or Dox. Also, selenium and v

Refinement of a differentiation protocol using neuroblastoma SH-SY5Y cells for use in neurotoxicology research

Since most models used to study neuronal dysfunction display disadvantages and ethical concerns, a fast and reproducible in vitro model to study mitochondria-related neurodegeneration is required. Here, we optimized and characterized a 3-day retinoic acid-based protocol to differentiate the SH-SY5Y cell line into a neuronal-like phenotype and investigated alterations in mitochondrial physiology an

Taurine and N-acetyl-cysteine supplementation prevents memory impairment in high-fat diet-fed female mice

Background: The risk to develop memory impairment in has been widely investigated in type 2 diabetes (T2D). There are several mechanisms proposed for T2D-associated cognitive impairment, such as brain insulin resistance, synaptic dysfunction, inflammation, gliosis, or disruption of neuron-astrocyte interactions (Garcia-Serrano & Duarte, 2020). On the other hand, supplementation with the antiox

Intracellular and Intercellular Mitochondrial Dynamics in Parkinson's Disease

The appearance of alpha-synuclein-positive inclusion bodies (Lewy bodies) and the loss of catecholaminergic neurons are the primary pathological hallmarks of Parkinson's disease (PD). However, the dysfunction of mitochondria has long been recognized as a key component in the progression of the disease. Dysfunctional mitochondria can in turn lead to dysregulation of calcium homeostasis and, especia

Phenolic wastewaters depuration by electrochemical oxidation process using Ti/IrO2 anodes

The electrochemical oxidation (EO) of phenolic wastewaters mimicking olive oil mill effluents was carried out in a batch stirring reactor using Ti/IrO2 anodes, varying the nature (NaCl and Na2SO4) and electrolyte concentration (1.8-20 g L-1), current density (57-119 mA cm(-2)) and initial pH (3.4-9). Phenolic content (TPh) and chemical oxygen demand (COD) removals were monitored as a function of a

Altered mitochondrial epigenetics associated with subchronic doxorubicin cardiotoxicity

Doxorubicin (DOX), a potent and broad-spectrum antineoplastic agent, causes an irreversible, cumulative and dose-dependent cardiomyopathy that ultimately leads to congestive heart failure. The mechanisms responsible for DOX cardiotoxicity remain poorly understood, but seem to involve mitochondrial dysfunction on several levels. Epigenetics may explain a portion of this effect. Since mitochondrial

Berberine-induced cardioprotection and Sirt3 modulation in doxorubicin-treated H9c2 cardiomyoblasts

Doxorubicin (DOX) is one of the most widely used anti-neoplastic agents. However, treatment with DOX is associated with cumulative cardiotoxicity inducing progressive cardiomyocyte death. Sirtuin 3 (Sirt3), a mitochondrial deacetylase, regulates the activity of proteins involved in apoptosis, autophagy and metabolism. Our hypothesis is that pharmacological modulation by berberine (BER) pre-conditi

Evaluation of biological properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride derivatives and their ability to inhibit hexokinase activity

This investigation has explored the properties of 3,3',4,4'-benzophenonetetracarboxylic dianhydride (BDTA) derivatives with regard to their being prospective inhibitors of hexokinase II (HKII). A pluripotent embryonic carcinoma cell line P19 (ECC), was used as the biological target for newly generated potential inhibitors of HKII. The results obtained from Virtual High-Throughput Screening (VHTS),

Targeting Mitochondria in Cardiovascular Diseases

BACKGROUND: Cardiovascular diseases (CVDs) are one of the main factors responsible for human morbidity and mortality. Since mitochondria play a critical role in the regulation of cardiac tissue homeostasis, this organelle is a critical target for the protective effects of several pharmaceuticals. Although specific mitochondria-targeted antioxidants and some pharmacological agents are described as

Ketogenic diets : from cancer to mitochondrial diseases and beyond

BACKGROUND: The employment of dietary strategies such as ketogenic diets, which force cells to alter their energy source, has shown efficacy in the treatment of several diseases. Ketogenic diets are composed of high fat, moderate protein and low carbohydrates, which favour mitochondrial respiration rather than glycolysis for energy metabolism.DESIGN: This review focuses on how oncological, neurolo

Methylglyoxal-Mediated Dopamine Depletion, Working Memory Deficit, and Depression-Like Behavior Are Prevented by a Dopamine/Noradrenaline Reuptake Inhibitor

Methylglyoxal (MGO) is an endogenous toxin, mainly produced as a by-product of glycolysis that has been associated to aging, Alzheimer's disease, and inflammation. Cell culture studies reported that MGO could impair the glyoxalase, thioredoxin, and glutathione systems. Thus, we investigated the effect of in vivo MGO administration on these systems, but no major changes were observed in the glyoxal

High Cholesterol Diet Exacerbates Blood-Brain Barrier Disruption in LDLr-/- Mice : Impact on Cognitive Function

BACKGROUND: Evidence has revealed an association between familial hypercholesterolemia and cognitive impairment. In this regard, a connection between cognitive deficits and hippocampal blood-brain barrier (BBB) breakdown was found in low-density lipoprotein receptor knockout mice (LDLr-/-), a mouse model of familial hypercholesterolemia.OBJECTIVE: Herein we investigated the impact of a hypercholes

Red wine consumption mitigates the cognitive impairments in low-density lipoprotein receptor knockout (LDLr-/-) mice

Although the benefits of moderate intake of red wine in decreasing incidence of cardiovascular diseases associated to hypercholesterolemia are well recognized, there are still widespread misconceptions about its effects on the hypercholesterolemia-related cognitive impairments. Herein we investigated the putative benefits of regular red wine consumption on cognitive performance of low-density lipo

LDL Receptor Deficiency Does not Alter Brain Amyloid-β Levels but Causes an Exacerbation of Apoptosis

Familial hypercholesterolemia (FH) is a genetic disorder caused by dysfunction of low density lipoprotein receptors (LDLr), resulting in elevated plasma cholesterol levels. FH patients frequently exhibit cognitive impairment, a finding recapitulated in LDLr deficient mice (LDLr-/-), an animal model of FH. In addition, LDLr-/- mice are more vulnerable to the deleterious memory impact of amyloid-β (

Leucine increases muscle mitochondrial respiration and attenuates glucose intolerance in diet-induced obesity in Swiss mice

Leucine is an essential amino acid that has been investigated by its participation in the regulation of whole-body metabolism and mitochondrial function. Here, we evaluated acute leucine effects on mitochondrial respiration of skeletal muscle from male Swiss mice in vitro. Additionally, we further investigated the effects of 4-wk leucine ingestion (2.5% on drinking water) on skeletal muscle mitoch

Decrement in resting and insulin-stimulated soleus muscle mitochondrial respiration is an early event in diet-induced obesity in mice

New Findings: What is the central question of this study? What are the temporal responses of mitochondrial respiration and mitochondrial responsivity to insulin in soleus muscle fibres from mice during the development of obesity and insulin resistance? What is the main finding and its importance? Short- and long-term feeding with a high-fat diet markedly reduced soleus mitochondrial respiration an