0000000000022975

AUTHOR

Sol Guerra-ojeda

showing 9 related works from this author

PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

2021

Abstract Background and aims Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodi…

medicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilationmedicine.disease_causeEnosmedicine.arteryInternal medicineAnimalsMedicineRenal arteryProtein kinase BSistema cardiovascularMetabolic SyndromeAortaDiabetisbiologybusiness.industryModels Theoreticalmedicine.diseasebiology.organism_classificationPPAR gammaVasodilationEndocrinologyEndothelium VascularRabbitsSodium nitroprussideMetabolic syndromeCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktOxidative stressmedicine.drugAtherosclerosis
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Relaxant and antiadrenergic effects of ranolazine in human saphenous vein.

2019

Abstract OBJECTIVES Ranolazine improves vascular function in animal models. We evaluate the effects of ranolazine on vascular function and adrenergic response in human saphenous vein. METHODS Rings from 53 patients undergoing coronary artery bypass grafting were mounted in organ baths. Concentration–response curves to ranolazine were constructed in rings precontracted with phenylephrine, endothelin-1, vasopressin, KCl and the thromboxane A2 analogue U-46619. In rings precontracted with phenylephrine, relaxation to ranolazine was tested in the absence and presence of endothelial factors inhibitors, K+ channel blockers and verapamil. The effects of ranolazine on frequency–response and concent…

Pulmonary and Respiratory MedicineAdrenergic AntagonistsCharybdotoxinAdrenergicRanolazine030204 cardiovascular system & hematologyPharmacologyNitric Oxide03 medical and health scienceschemistry.chemical_compoundPotassium Channels Calcium-Activated0302 clinical medicineRanolazineMedicineAnimalsHumansChannel blockerSaphenous Vein030212 general & internal medicinePhenylephrineTetraethylammoniumbusiness.industryGeneral MedicineNG-Nitroarginine Methyl EsterchemistryVerapamilSurgeryEndothelium Vascularmedicine.symptomCardiology and Cardiovascular MedicinebusinessVasoconstrictionmedicine.drugEuropean journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
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Astrocytes Protect Neurons from Aβ1-42 Peptide-Induced Neurotoxicity Increasing TFAM and PGC-1 and Decreasing PPAR-γ and SIRT-1

2015

One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated re…

MnSODProgrammed cell deathPPAR-γPeroxisome proliferator-activated receptorMitochondrionBiologyBioinformaticsmedicine.disease_causeAlzheimer's DiseaseNeurologiaPGC-1Sirtuin 1medicineAnimalsTFAMCells Culturedchemistry.chemical_classificationNeuronsAmyloid beta-PeptidesCell DeathSirtuin 1Caspase 3Superoxide DismutaseNeurotoxicityTranscription Factor RelAGeneral MedicineTFAMmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCoculture TechniquesPeptide FragmentsCell biologyMitochondriaPeroxidesRatsPPAR gammachemistryMitochondrial biogenesisNF-κB.Astrocytesbiology.proteinFisiologia humanaLipid PeroxidationOxidative stressResearch PaperTranscription FactorsInternational Journal of Medical Sciences
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Effects of photodynamic therapy in periodontal treatment: A randomized, controlled clinical trial

2017

Aim To evaluate the effects of photodynamic therapy (PDT) in the nonsurgical treatment of chronic periodontitis. Materials and methods A randomized, single-blind, controlled, parallel-group clinical trial was performed. Sixty patients were enrolled: 20 healthy controls and 40 patients with periodontitis. The 40 patients were randomized for scaling and root planing (SRP) or SRP+PDT. Periodontal (plaque index, probing depth, clinical recession, clinical attachment level, bleeding on probing, and gingival crevicular fluid volume, corresponding to 381 vs 428 critical sites), microbiological (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema dentico…

AdultMale0301 basic medicine030103 biophysicsmedicine.medical_specialtyBleeding on probingDentistryenvironment and public healthGastroenterologyRoot Planing03 medical and health sciences0302 clinical medicineScaling and root planingInternal medicinemedicineHumansTannerella forsythiaSingle-Blind MethodAgedPeriodontitisbiologybusiness.industryPrevotella intermediaAggregatibacter actinomycetemcomitansCampylobacter rectus030206 dentistryMiddle Agedbiology.organism_classificationmedicine.diseaseChronic periodontitisTreatment OutcomePhotochemotherapyChronic PeriodontitisDental ScalingPeriodonticsFemalePeriodontal Indexmedicine.symptombusinessBiomarkersJournal of Clinical Periodontology
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Changes in Chemokines and Chemokine Receptors Expression in a Mouse Model of Alzheimer's Disease

2018

The amyloid precursor protein plus presenilin-1 (APP/PS1) mice are a frequently-used model for Alzheimer's disease studies (AD). However, the data relevant to which proteins are involved in inflammatory mechanism are not sufficiently well-studied using the AD mouse model. Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PS1 and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDF1 intervenes normally in the transport across cell membranes and both were found …

ChemokineCCL3CCL1CCR8BiologyApplied Microbiology and BiotechnologyReceptors CCR8Mice03 medical and health sciencesChemokine receptorAlzheimer DiseaseGlial Fibrillary Acidic Proteinmental disordersmedicineAmyloid precursor proteinAnimalsChemokine CCL4Molecular BiologyEcology Evolution Behavior and SystematicsChemokine CCL3030304 developmental biologyInflammation0303 health scienceschemokine receptors chemotaxis inflammation behaviorHand StrengthChemotaxisChemotaxisCell BiologyAlzheimer's diseaseCell biologyGliosisbiology.proteinReceptors ChemokineChemokinesmedicine.symptomResearch PaperDevelopmental BiologyInternational Journal of Biological Sciences
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Neuronal effects of Sugammadex in combination with Rocuronium or Vecuronium.

2017

Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these…

vecuroniumNecrosisEstrès oxidatiuPrimary Cell CulturerocuroniumCaspase 3NeuronesPharmacologySugammadexSugammadex03 medical and health sciences0302 clinical medicine030202 anesthesiologymedicineAnimalsHumansAndrostanolsRocuroniumCell damageNeuronsVecuronium BromideDose-Response Relationship DrugCaspase 3business.industryapoptosis.Apoptosis Inducing FactorCytochromes c030208 emergency & critical care medicineGeneral Medicinemedicine.diseaseneuronRatsDrug Combinationsmedicine.anatomical_structureGene Expression RegulationApoptosisToxicityNeuronNeuromuscular Blocking Agentsmedicine.symptombusinessResearch Papergamma-Cyclodextrinsmedicine.drug
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Effects of Ranolazine on Astrocytes and Neurons in Primary Culture.

2016

Ranolazine (Rn) is an antianginal agent used for the treatment of chronic angina pectoris when angina is not adequately controlled by other drugs. Rn also acts in the central nervous system and it has been proposed for the treatment of pain and epileptic disorders. Under the hypothesis that ranolazine could act as a neuroprotective drug, we studied its effects on astrocytes and neurons in primary culture. We incubated rat astrocytes and neurons in primary cultures for 24 hours with Rn (10-7, 10-6 and 10-5 M). Cell viability and proliferation were measured using trypan blue exclusion assay, MTT conversion assay and LDH release assay. Apoptosis was determined by Caspase 3 activity assay. The …

0301 basic medicineMacroglial CellsPhysiologyInterleukin-1betaProtein ExpressionCell Culture Techniqueslcsh:MedicineApoptosisPharmacologyPathology and Laboratory Medicine0302 clinical medicineRanolazineAnimal CellsImmune PhysiologyMedicine and Health SciencesEnzyme assaysColorimetric assaysEnzyme-Linked Immunoassayslcsh:ScienceBioassays and physiological analysisImmune ResponseNeuronsInnate Immune SystemMultidisciplinaryMTT assayCell DeathCaspase 3medicine.anatomical_structureCell ProcessesCytokinesTumor necrosis factor alphaCellular TypesAstrocyteResearch ArticleProgrammed cell deathCell SurvivalImmunologyCaspase 3Glial CellsBiologyGene Expression Regulation EnzymologicMitochondrial Proteins03 medical and health sciencesSigns and SymptomsmedicineGene Expression and Vector TechniquesAnimalsMTT assayViability assayMolecular Biology TechniquesImmunoassaysMolecular BiologyInflammationMolecular Biology Assays and Analysis TechniquesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RBiology and Life SciencesCell BiologyMolecular DevelopmentRatsPPAR gammaResearch and analysis methodsOxidative Stress030104 developmental biologyCell cultureApoptosisAstrocytesImmune SystemBiochemical analysisImmunologic Techniqueslcsh:QFisiologia humanaApoptosis Regulatory ProteinsCarrier Proteins030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβ1-42 on Astrocytes in primary culture

2020

Aspirin has been used as anti-inflammatory and anti-aggregate for decades but the precise mechanism(s) of action after the presence of the toxic peptide Aβ1-42 in cultured astrocytes remains poorly resolved. Here we use low-doses of aspirin (10-7 M) in astrocytes in primary culture in presence or absence of Aβ1-42 toxic peptide. We noted an increase of cell viability and proliferation with or without Aβ1-42 peptide presence in aspirin treated cells. In addition, a decrease in apoptosis, determined by Caspase 3 activity and the expression of Cyt c and Smac/Diablo, were detected. Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-β and TNF-α) and NF-ᴋB prot…

chemistry.chemical_classificationAspirinNecrosisbiologyCytochrome cPeroxisome proliferator-activated receptorInflammationGeneral MedicinePharmacologymedicine.disease_cause03 medical and health sciences0302 clinical medicinechemistryApoptosismedicinebiology.protein030211 gastroenterology & hepatologyViability assaymedicine.symptomOxidative stressmedicine.drugInternational Journal of Medical Sciences
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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