Search results for "inflammation"

showing 10 items of 2662 documents

GABA-containing compound gammapyrone protects against brain impairments in Alzheimer's disease model male rats and prevents mitochondrial dysfunction…

2018

Neuroinflammation, oxidative stress, decreased glucose/energy metabolism, and disrupted neurotransmission are changes that occur early in sporadic Alzheimer's disease (AD), manifesting as mild cognitive impairment. Recently, the imbalanced function of the gamma-aminobutyric acid (GABA) system was identified as a critical factor in AD progression. Thus, maintaining balance among neurotransmitter systems, particularly the GABA system, can be considered a beneficial strategy to slow AD progression. The present study investigated the effects of the compound gammapyrone, a molecule containing three GABA moieties: "free" moiety attached to the position 4 of the 1,4-dihydropyridine (DHP) ring, and…

0301 basic medicineMalemedicine.medical_specialtyAllosteric regulationbioenergetics; GABA; intracerebroventricular streptozocin; PC12 cells; protein expression; spatial learning/memoryNeurotransmissionspatial learning/memorymedicine.disease_causebioenergeticsNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceGABA0302 clinical medicineReceptors GABAAlzheimer DiseaseMemoryInternal medicinemedicineAnimalsRats WistarReceptorMaze Learningprotein expressionNeuroinflammationCells Culturedgamma-Aminobutyric AcidGABAA receptorChemistryGlutamate DecarboxylasePC12 cellsBrainintracerebroventricular streptozocinMitochondriaStreptozocinDisease Models Animal030104 developmental biologyEndocrinologyNeuroprotective AgentsAstrocytesAcetylcholinesteraseEncephalitisMicroglia030217 neurology & neurosurgeryOxidative stressJournal of neuroscience research
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Angiotensin II type II receptors and colonic dysmotility in 2,4-dinitrofluorobenzenesulfonic acid-induced colitis in rats

2016

Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a l…

0301 basic medicineMalemedicine.medical_specialtyAngiotensin receptormedicine.drug_classColonPhysiologyInflammationAT2 receptorReceptor Angiotensin Type 2Bowel inflammationEndocrine and Autonomic SystemContractilityRenin-Angiotensin System03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsRats WistarReceptorAngiotensin II receptor type 1Endocrine and Autonomic SystemsChemistryAT1 receptorAngiotensin IIMuscle contractilityGastroenterologyMuscle SmoothNitric oxideReceptor antagonistColitisAngiotensin II030104 developmental biologyEndocrinologyLosartancardiovascular system030211 gastroenterology & hepatologyDinitrofluorobenzenemedicine.symptomGastrointestinal Motilityhormones hormone substitutes and hormone antagonistsmedicine.drugMuscle Contraction
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Glucagon-like peptide-2 reduces the obesity-associated inflammation in the brain.

2018

Growing evidence suggests a link between obesity and neurodegeneration. The purpose of the present study was to explore the neuroprotective potential of glucagon-like peptide-2 (GLP-2) in the brain of high fat diet (HFD)-fed mice. Markers of inflammation and oxidative stress were analysed in the brains of obese mice chronically treated with [Gly2]-GLP-2 (teduglutide), the stable analogue of the GLP-2, and they were compared to age-matched untreated obese and lean animals. Neurodegeneration was examined by TUNEL assay. HFD feeding increased the expression of pro-inflammatory mediators (NF-kB, IL-8, TNF-α, IL-1β and IL-6), glial fibrillary acidic protein (GFAP), index of gliosis and neurodege…

0301 basic medicineMalemedicine.medical_specialtyInflammationmedicine.disease_causeDiet High-FatSettore BIO/09 - FisiologiaNeuroprotectionlcsh:RC321-57103 medical and health sciences0302 clinical medicineNeuroinflammationInternal medicinemedicineGlucagon-Like Peptide 2AnimalsObesityNeurodegenerationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationTUNEL assayGlial fibrillary acidic proteinbiologyChemistryNeurodegenerationdigestive oral and skin physiologyBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyNeuroprotective AgentsNeurologyGliosisOxidative stressAstrocytesbiology.proteinGlucagon-Like Peptide-2 ReceptorOxidative streEncephalitismedicine.symptomInflammation MediatorsGLP-2030217 neurology & neurosurgeryOxidative stresshormones hormone substitutes and hormone antagonistsNeurobiology of disease
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Activation of MORs in the VTA induces changes on cFos expression in different projecting regions: Effect of inflammatory pain.

2019

Abstract Chronic pain is a worldwide major health problem and many pain-suffering patients are under opioid based therapy. Epidemiological data show that pain intensity correlates with the risk of misuse of prescription opioids, and other drugs of abuse including alcohol. This increased vulnerability to suffer Substance Use Disorders could be, in part, caused by functional changes that occur over the mesocorticolimbic system, a brain pathway involved in reward processing and addiction. Previous data in rats revealed that inflammatory pain desensitizes mu opioid receptors (MORs) in the ventral tegmental area (VTA). As a consequence, pain alters dopamine release in the nucleus accumbens (NAc)…

0301 basic medicineMalemedicine.medical_specialtyMicroinjectionsFreund's AdjuvantReceptors Opioid muPainNucleus accumbens03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineDopamineInternal medicinemental disordersNeural PathwaysMedicineAnimalsInflammationbusiness.industryVentral Tegmental AreaChronic painGenes fosCell BiologyEnkephalin Ala(2)-MePhe(4)-Gly(5)-medicine.diseaseImmunohistochemistryRatsVentral tegmental areaAnalgesics OpioidDAMGOStria terminalis030104 developmental biologymedicine.anatomical_structureEndocrinologynervous systemchemistryOpioidGene Expression Regulationbusiness030217 neurology & neurosurgerymedicine.drugBasolateral amygdalaNeurochemistry international
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Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
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Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model.

2019

Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer’s as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effe…

0301 basic medicineMalemedicine.medical_specialtyNeurologyAmyloidTraumatic brain injuryPlaque AmyloidProtein Aggregation PathologicalS100A9Proinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsCalgranulin BSignificant riskNeuroinflammationNeuronsbusiness.industryGeneral NeuroscienceBrainmedicine.diseasenervous system diseasesDisease Models Animal030104 developmental biologyMicrogliabusinessAlzheimer’s disease Amyloid Neuroinflammation Oligomerization S100A9 Traumatic brain injuryNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction.

2016

Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from ad…

0301 basic medicineMalemedicine.medical_specialtyTime FactorsGalectin 3Myocardial InfarctionInflammationCoronary Artery Disease030204 cardiovascular system & hematologyAMICoronary artery disease03 medical and health sciences0302 clinical medicineFibrosisInternal medicineMedicineHumansCADcardiovascular diseasesMyocardial infarctionPlaqueAgedInflammationbusiness.industryMedicine (all)Mean ageGeneral MedicineMiddle Agedmedicine.disease030104 developmental biologyGalectin-3ImmunologyCardiologyBiomarker (medicine)Femalemedicine.symptombusinessBiomarkersArchives of medical research
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Effect of chondroitin sulphate on synovitis of knee osteoarthritic patients.

2017

Abstract Objective To evaluate by ultrasonography the effect of chondroitin sulfate (CS) on synovitis in patients with knee osteoarthritis (KOA). To collaborate in the understanding of the biochemical mechanisms involved in the synovial inflammation process. Methods Randomized, single-blind, controlled trial involving 70 patients with primary KOA treated for 6 months with CS or acetaminophen (ACT). Evaluation of KOA status at baseline, 6 weeks, 3 and 6 months included: ultrasonography to assess synovitis (following the OMERACT expertise group definition), visual analogue scale and Lequesne index to measure pain and function, and ELISA to quantify inflammatory mediators in serum and synovial…

0301 basic medicineMalemedicine.medical_specialtyVisual analogue scaleInflammationPilot ProjectsOsteoarthritisGastroenterologylaw.invention03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRandomized controlled triallawInternal medicineSynovitisMedicineSynovial fluidHumansSingle-Blind MethodChondroitin sulfateAcetaminophenAgedPain MeasurementUltrasonography030203 arthritis & rheumatologyAged 80 and overSynovitisbusiness.industryAnti-Inflammatory Agents Non-SteroidalChondroitin SulfatesMiddle AgedOsteoarthritis Kneemedicine.diseaseAcetaminophenBiomechanical Phenomena030104 developmental biologyTreatment OutcomechemistryFemalemedicine.symptombusinessBiomarkersmedicine.drugFollow-Up StudiesMedicina clinica
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Changes in CDKN2A/2B expression associate with T-cell phenotype modulation in atherosclerosis and type 2 diabetes mellitus.

2018

Previous studies indicate a role of CDKN2A/2B/2BAS genes in atherosclerosis and type 2 diabetes mellitus (T2DM). Progression of these diseases is accompanied by T-cell imbalance and chronic inflammation. Our main objective was to investigate a potential association between CDKN2A/2B/2BAS gene expression and T cell phenotype in T2DM and coronary artery disease (CAD) in humans, and to explore the therapeutic potential of these genes to restore immune cell homeostasis and disease progression. Reduced mRNA levels of CDKN2A (p16Ink4a), CDKN2B (p15Ink4b), and CDKN2BAS were observed in human T2DM and T2DM-CAD subjects compared with controls. Protein levels of p16Ink4a and p15Ink4b were also dimini…

0301 basic medicineMalemedicine.medical_specialtyendocrine system diseasesMice Knockout ApoECD3T cellCD14Inflammation03 medical and health sciencesMice0302 clinical medicinePhysiology (medical)Internal medicineNeointimamedicineAnimalsHumansIL-2 receptorInterleukin-7 receptorneoplasmsbiologybusiness.industryGenes p16Biochemistry (medical)CDKN2BASPublic Health Environmental and Occupational HealthType 2 Diabetes MellitusGeneral MedicineAtherosclerosis030104 developmental biologyEndocrinologymedicine.anatomical_structureDiabetes Mellitus Type 2030220 oncology & carcinogenesisbiology.proteinLeukocytes Mononuclearmedicine.symptombusinessTranslational research : the journal of laboratory and clinical medicine
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Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

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0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
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