Search results for "Inflammation."

showing 10 items of 2627 documents

Cytotoxic effects of oxysterols associated with human diseases: Induction of cell death (apoptosis and/or oncosis), oxidative and inflammatory activi…

2009

Oxysterols resulting from spontaneous or enzymatic oxidation of cholesterol are present in numerous foodstuffs and have been identified at increased levels in the plasma and the vascular walls of patients with cardiovascular diseases, especially in atherosclerotic lesions. Consequently, their role in lipid disorders is widely suspected, but they may also contribute to the development of important degenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, osteoporosis, age-related macular degeneration, and cataract. Since these pathologies can be associated with the presence of apoptotic cells, oxidative and inflammatory processes, and lipid disorders, the ab…

Programmed cell deathClinical BiochemistryInflammationApoptosisOxidative phosphorylationPharmacologyBiologyLipidosesBiochemistrychemistry.chemical_compoundMacular DegenerationNeoplasmspolycyclic compoundsmedicineCytotoxic T cellHumansMolecular BiologyKetocholesterolsPhospholipidsPhospholipidosisInflammationCholesterolGeneral MedicineAtherosclerosisHydroxycholesterolsOxidative StresschemistryApoptosisImmunologyMolecular Medicinelipids (amino acids peptides and proteins)Signal transductionmedicine.symptomMolecular aspects of medicine
researchProduct

Involvement of Microglia in Neurodegenerative Diseases: Beneficial Effects of Docosahexahenoic Acid (DHA) Supplied by Food or Combined with Nanoparti…

2021

Neurodegenerative diseases represent a major public health issue and require better therapeutic management. The treatments developed mainly target neuronal activity. However, an inflammatory component must be considered, and microglia may constitute an important therapeutic target. Given the difficulty in developing molecules that can cross the blood–brain barrier, the use of food-derived molecules may be an interesting therapeutic avenue. Docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid (22:6 omega-3), has an inhibitory action on cell death and oxidative stress induced in the microglia. It also acts on the inflammatory activity of microglia. These data obtained in vitro or…

Programmed cell deathDocosahexaenoic AcidsQH301-705.5microgliaApoptosisInflammationReviewPharmacologyProtective AgentsInhibitory postsynaptic potentialmedicine.disease_causeCatalysisInorganic ChemistryDrug Delivery Systemsneurodegenerative diseasemedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopychemistry.chemical_classificationMicrogliabusiness.industryOrganic ChemistryNeurodegenerative DiseasesGeneral Medicinedocosahexaenoic acidnanomedicineIn vitroComputer Science ApplicationsDisease Models AnimalOxidative StressChemistryTreatment Outcomemedicine.anatomical_structurechemistryBlood-Brain BarrierinflammationDocosahexaenoic acidDietary SupplementsNanoparticlesmedicine.symptombusinessOxidative stressPolyunsaturated fatty acidInternational Journal of Molecular Sciences
researchProduct

Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
researchProduct

P7142-AG impacts on endothelial cell activation and endothelial cell viability in vitro and impairs endothelial repair in vivo

2019

Abstract Background The endocannabinoid (eCB) 2-arachidonoylglycerol (2-AG) is a known modulator of inflammation and few studies have addressed its influence on myeloid cells in the context of atherogenesis. However, the impact of 2-AG on endothelial cell function has not been studied before. Methods Endothelial repair was studied in two treatment groups of wildtype mice following electrical denudation of the common carotid artery at a length of 3000 μm. One group received the monoacylglycerol lipase (MAGL)-inhibitor JZL184 [5 mg/kg i.p.], which impairs 2-AG degradation and thus causes elevated 2-AG levels, the other group received vehicle. The residual endothelial gap at five days in eithe…

Programmed cell deathEndotheliumbusiness.industrymedicine.medical_treatmentInflammationIn vitroCell biologyEndothelial stem cellmedicine.anatomical_structureCytokineIn vivomedicineTHP1 cell linemedicine.symptomCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
researchProduct

Role of caspase-8 in hepatocyte response to infection and injury in mice.

2007

Caspase-8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase-8 gene specifically in the liver, we found that caspase-8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes, attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the…

Programmed cell deathInflammationCaspase 8MiceConditional gene knockoutmedicineAnimalsListeriosisCaspaseCell ProliferationInflammationMice KnockoutCaspase 8HepatologybiologyCell DeathCell growthLiver Regenerationmedicine.anatomical_structureHepatocyteImmunologyCancer researchChronic inflammatory responsebiology.proteinHepatocytesmedicine.symptomHepatology (Baltimore, Md.)
researchProduct

Prevention of 7-ketocholesterol-induced side effects by natural compounds

2018

Cholesterol oxidation products, also named oxysterols, can be formed either by cholesterol auto-oxidation, enzymatically or both. Among these oxysterols, 7-ketocholesterol (7KC) is mainly formed during radical attacks that take place on the carbon 7 of cholesterol. As increased levels of 7KC have been found in the tissues, plasma and/or cerebrospinal fluid of patients with major diseases, especially age-related diseases (cardiovascular diseases, eye diseases, neurodegenerative diseases), some cancers, and chronic inflammatory diseases, it is suspected that 7KC, could contribute to their development. Since 7KC, provided by the diet or endogenously formed, is not or little efficiently metabol…

Programmed cell deathOxysterol030309 nutrition & dieteticsTocopherolsInflammationPharmacologymedicine.disease_causeAntioxidantsIndustrial and Manufacturing Engineering03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologymedicineHumansNoncommunicable DiseasesKetocholesterolsInflammation0303 health sciencesCholesterolFatty AcidsPolyphenols04 agricultural and veterinary sciencesGeneral Medicine040401 food scienceCytoprotectionOxidative StressMetabolic pathwaychemistryHepatic stellate cellmedicine.symptomOxidation-ReductionOxidative stressFood ScienceCritical Reviews in Food Science and Nutrition
researchProduct

Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis

2011

Two groups identify the regulation of death-receptor-induced necroptosis as an epithelial intrinsic mechanism that is important for the maintenance of immune homeostasis and the prevention of intestinal inflammation in mice. Welz et al. describe an unexpected physiological function for FADD (Fas-associated protein with death domain), an adaptor protein required for death-receptor-induced apoptosis. Mice with intestinal epithelial specific knockout of FADD develop severe colon inflammation due to increased death of FADD-deficient colonic epithelial cells. Gunther et al. report a novel and unexpected function of caspase-8 in maintaining immune homeostasis in the gut. Caspase-8 expression by g…

Programmed cell deathPaneth CellsNecroptosisInflammationApoptosisBiologyIn Vitro Techniquesdigestive systemArticle03 medical and health sciencesMiceNecrosis0302 clinical medicineCrohn DiseasemedicineAnimalsHumansFADD030304 developmental biology0303 health sciencesCaspase 8MultidisciplinaryInnate immune systemTumor Necrosis Factor-alphaColitisIntestinal epithelium3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesPaneth cellImmunologybiology.proteinCancer researchTumor necrosis factor alphaGoblet Cellsmedicine.symptomGene DeletionNature
researchProduct

Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxi…

Programmed cell deathParkinson's diseaseInflammationReviewDiseasePharmacologyMitochondrionmedicine.disease_causelipids nutrientsCatalysislcsh:ChemistryInorganic ChemistrysynucleinFish OilsAlzheimer DiseaseHumansPlant OilsMedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopybusiness.industryFatty AcidsOrganic ChemistryapoptosisamyloidParkinson DiseaseNutrientsGeneral Medicinemedicine.diseaseLipidsCytoprotectionComputer Science ApplicationsmitochondriaOxidative Stresslcsh:Biology (General)lcsh:QD1-999CytoprotectionParkinson’s diseaseSynucleinTaumedicine.symptombusinessAlzheimer’s diseaseOxidative stressInternational Journal of Molecular Sciences
researchProduct

Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo.

2009

Abstract Background and purpose HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro . Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo . Materials and methods Four hours to 24h after total body irradiation (6Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5Gy and analyses were performed 3weeks after the first radiation treatment. Molecular markers of inflammation and f…

Programmed cell deathPathologymedicine.medical_specialtyStatinmedicine.drug_classCell SurvivalPharmacologyRadiation DosageMiceRandom AllocationIn vivoFibrosisReference ValuesRadiation IonizingmedicineAnimalsHumansRadiology Nuclear Medicine and imagingLovastatinRNA MessengerRadiation InjuriesLungProbabilityMice Inbred BALB CChemistryTumor Necrosis Factor-alphaNF-kappa BDose-Response Relationship RadiationHematologymedicine.diseaseCTGFIntestinesDisease Models AnimalRadiation Injuries ExperimentalOncologyLiverApoptosisToxicitylipids (amino acids peptides and proteins)FemaleLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammation Mediatorsmedicine.drugDNA DamageRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
researchProduct

Side effects of oxysterols: cytotoxicity, oxidation, inflammation, and phospholipidosis.

2008

Oxysterols are 27-carbon atom molecules resulting from autoxidation or enzymatic oxidation of cholesterol. They are present in numerous foodstuffs and have been demonstrated to be present at increased levels in the plasma of patients with cardiovascular diseases and in atherosclerotic lesions. Thus, their role in lipid disorders is widely suspected, and they might also be involved in important degenerative diseases such as Alzheimer's disease, osteoporosis, and age-related macular degeneration. Since atherosclerosis is associated with the presence of apoptotic cells and with oxidative and inflammatory processes, the ability of some oxysterols, especially 7-ketocholesterol and 7β-hydrox…

Programmed cell deathPhysiologyImmunologyBiophysicsInflammationApoptosisOxidative phosphorylationPharmacologyLipidosesBiochemistryPhospholipidosischemistry.chemical_compoundmedicinepolycyclic compoundsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicitylcsh:QH301-705.5PhospholipidsPhospholipidosisInflammationlcsh:R5-920ChemistryCholesterolGeneral NeuroscienceCell BiologyGeneral MedicineOxysterolsAtherosclerosisHydroxycholesterolsBiochemistrylcsh:Biology (General)Apoptosislipids (amino acids peptides and proteins)medicine.symptomSignal transductionlcsh:Medicine (General)Oxidation-ReductionBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
researchProduct