Search results for "CXCL"

showing 8 items of 98 documents

3′-Demethyldihydromaldoxin and dihydromaldoxin, two anti-inflammtory diaryl ethers from a Steganospora species

2012

CXCL10 (IP-10) is a highly inducible chemoattractant, which contributes to the recruitment of inflammatory cells such as macrophages and T-lymphocytes and thereby has important roles in chronic inflammatory conditions. In a search for new inhibitors of CXCL10 expression in MonoMac6 (MM6) cells, the new diaryl ether 3'-demethyldihydromaldoxin (1) along with the known compound dihydromaldoxin (2), were isolated from fermentations of a Steganospora species. The structures of the compounds were elucidated by a combination of one- and two-dimensional NMR spectroscopy and mass spectrometry. Compounds (1) and (2) inhibited lipopolysaccharide (LPS)/interferon-γ (IFN-γ)-induced CXCL10 promoter activ…

Spectrometry Mass Electrospray IonizationLipopolysaccharideCell SurvivalAntiparasiticmedicine.drug_classAnti-Inflammatory AgentsBiologyTransfectionCell LineInhibitory Concentration 50Lactoneschemistry.chemical_compoundBiosynthesisInterferonDrug DiscoverymedicineProtein biosynthesisAnimalsHumansCXCL10Spiro CompoundsNuclear Magnetic Resonance BiomolecularPharmacologyDose-Response Relationship DrugMolecular StructurePhenyl EthersFungiChemotaxisTransfectionChemokine CXCL10chemistryBiochemistrymedicine.drugThe Journal of Antibiotics
researchProduct

ChemInform Abstract: Ganodermycin, a Novel Inhibitor of CXCL10 Expression from Ganoderma applanatum.

2012

Ganodermycin (I), a novel inhibitor of CXCL10 expression, is isolated from Ganoderma applanatum.

TerpeneGanoderma applanatumbiologyBiochemistryimmune system diseasesChemistryvirus diseasesCXCL10hemic and immune systemsGeneral Medicinerespiratory systembiology.organism_classificationChemInform
researchProduct

The C-X-C Motif Chemokine Ligand 1 Sustains Breast Cancer Stem Cell Self-Renewal and Promotes Tumor Progression and Immune Escape Programs

2021

Breast cancer (BC) mortality is mainly due to metastatic disease, which is primarily driven by cancer stem cells (CSC). The chemokine C-X-C motif ligand-1 (CXCL1) is involved in BC metastasis, but the question of whether it regulates breast cancer stem cell (BCSC) behavior is yet to be explored. Here, we demonstrate that BCSCs express CXCR2 and produce CXCL1, which stimulates their proliferation and self-renewal, and that CXCL1 blockade inhibits both BCSC proliferation and mammosphere formation efficiency. CXCL1 amplifies its own production and remarkably induces both tumor-promoting and immunosuppressive factors, includingSPP1/OPN,ACKR3/CXCR7,TLR4,TNFSF10/TRAILandCCL18and, to a lesser exte…

breast cancer stem cellsQH301-705.5animal diseasesSettore MED/50 - Scienze Tecniche Mediche ApplicatechemokinesBiologyCXCR4MetastasisCell and Developmental Biologyimmunity geneCancer stem cellmedicinetumor microenvironmentCXC chemokine receptorsBiology (General)immunity genesTriple-negative breast cancerTumor microenvironmentbreast cancer stem cellchemokineCell BiologyBrief Research Reportrespiratory systemmedicine.diseaseCXCL1Tumor progressiontriple-negative breast cancerCancer researchCCL28Settore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioDevelopmental BiologyFrontiers in Cell and Developmental Biology
researchProduct

Disfunción endotelial en territorio arterial en pacientes jóvenes con enfermedad tromboembólica venosa

2015

La enfermedad tromboembólica venosa es la patología vascular más frecuente en gente joven, con 70 casos por cada 100.000 habitantes/año. En los últimos años se ha visto asociada al desarrollo de patología arterial, lo que aumenta aún más su morbimortalidad con una amplia repercusión socioeconómica. Este hecho ha sido objeto de diferentes estudios, sin que los mecanismos por los cuales se produce esta asociación entre patología venosa y arterial hayan sido del todo elucidados, sugiriéndose una etiopatogenia común principalmente basada en el estado inflamatorio que subyace en ambas patologías. Por ello, el objetivo del presente trabajo lo ha constituido el estudio de la inflamación vascular a…

disfuncion endotelialUNESCO::CIENCIAS MÉDICAS:CIENCIAS MÉDICAS [UNESCO]trombosis venosafractalquinaCXCL16
researchProduct

Chronic aspartame intake causes deficient glutathione synthesis and induces cxcl1 up-regulation in mice liver

2018

Reduced glutathione (GSH) depletion and inflammation have been linked to chronic aspartame consumption. However, the cause of aspartame-induced GSH depletion and the role of pro- and anti-inflammatory cytokines in aspartame-triggered inflammation are still unknown. The aims of this research were to investigate if aspartame causes GSH depletion due to deficient synthesis and also which pro- and anti-inflammatory genes are involved in aspartame-related inflammation in mice liver. Mice were divided into three groups: control, aspartame (80 mg kg-1, v.o., 3 months), aspartame treated with N-acetylcysteine (NAC) (1 mmol kg-1, i.p., last month). Aspartame markedly reduced GSH, γ-glutamylcysteine …

medicine.medical_specialtyAspartameInflammationGlutathioneBiochemistryCXCL1chemistry.chemical_compoundGCLCEndocrinologychemistryDownregulation and upregulationPhysiology (medical)Internal medicineMolemedicinemedicine.symptomCysteineFree Radical Biology and Medicine
researchProduct

Combined sub-optimal doses of Rosuvastatin and Bexarotene impairs angiotensin II-induced arterial mononuclear cell adhesion through inhibition of Nox…

2015

Aim: Mononuclear cell (MC) infiltration into the arterial subendothelium is a key event in atherogenesis. Rosuvastatin (Rosu) and bexarotene (Bex) exert anti-inflammatory activity, but serious dose-related adverse effects have emerged. The need for safer and effective strategies to prevent and treat atherosclerosis led us to test the effect of combined use of both drugs on angiotensin II (Ang-II)-induced arterial MC recruitment. Results: Vehicle, Rosu (10–30 nM), Bex (0.3–1 μM), or a combination of both were administered to human umbilical arterial endothelial cells (HUAECs) 20 h before stimulation with 1 μM Ang-II (4 h). Surprisingly, a combination of Rosu (10 nM)+Bex (0.3 μM), which did n…

medicine.medical_specialtyTetrahydronaphthalenesPhysiologyPeroxisome Proliferator-Activated ReceptorsClinical BiochemistryCCL2BiologyNitric OxideBiochemistryPeripheral blood mononuclear cellCell LineInternal medicineCell AdhesionmedicineAnticarcinogenic AgentsHumansRosuvastatinInterleukin 8Rosuvastatin CalciumMolecular BiologyGeneral Environmental ScienceSistema cardiovascularBexaroteneSulfonamidesDiabetisArtèriesAngiotensin IIMembrane ProteinsNADPH OxidasesArteriesCell BiologyAngiotensin IIFluorobenzenesCXCL1Original Research CommunicationsPyrimidinesRetinoid X ReceptorsEndocrinologyNADPH Oxidase 5BexaroteneLeukocytes MononuclearGeneral Earth and Planetary SciencesSignal transductionSignal Transductionmedicine.drug
researchProduct

Peripheral blood levels of CXCL10 are a useful marker for diabetic polyneuropathy in subjects with type 2 diabetes.

2020

BACKGROUND Diabetic peripheral neuropathy (DPN) is a chronic complication of diabetes mellitus associated with high morbidity and mortality. Major risk factors for DPN include metabolic changes, duration of diabetes, nerve ischaemia and derangements in regeneration and nerve repair programmes. Chemokines have been previously implicated in the pathogenesis of various neuropathies and neuropathic pain processes. The aim of this pilot study was to evaluate the association between the plasma levels of chemokines (CXCL9, CXCL10 and CXCL11) in the presence of DPN in a cohort of type 2 diabetes (T2D) patients. MATERIALS AND METHODS We studied 73 patients with T2D: 36 with DPN and 37 without DPN. D…

medicine.medical_specialtybusiness.industryPilot ProjectsGeneral MedicineType 2 diabetesmedicine.diseaseGastroenterologyChemokine CXCL10Peripheral neuropathyDiabetes Mellitus Type 2Diabetic NeuropathiesRisk FactorsInternal medicineDiabetes mellitusNeuropathic painmedicineCXCL10CXCL9HumansCXCL11ComplicationbusinessBiomarkersInternational journal of clinical practiceREFERENCES
researchProduct

Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
researchProduct