Search results for "4 inhibitors"

showing 10 items of 21 documents

Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors

2015

Introduction This work was undertaken to delineate intracellular signaling pathways for the PDE4 inhibitor apremilast and to examine interactions between apremilast, methotrexate and adenosine A2A receptors (A2AR). Methods After apremilast and LPS incubation, intracellular cAMP, TNF-α, IL-10, IL-6 and IL-1α were measured in the Raw264.7 monocytic murine cell line. PKA, Epac1/2 (signaling intermediates for cAMP) and A2AR knockdowns were performed by shRNA transfection and interactions with A2AR and A2BR, as well as with methotrexate were tested in vitro and in the murine air pouch model. Statistical differences were determined using one or two-way ANOVA or Student’s t test. The alpha nominal…

MaleAdenosineReceptor Adenosine A2AImmunologyBlotting WesternAdenosine A2A receptorGene ExpressionPharmacologyBiologyCell LineMiceRheumatologyPhenethylaminesmedicineCyclic AMPImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsReceptorIC50ArtritisReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesAdenosineMolecular biologyCyclic AMP-Dependent Protein KinasesThalidomideMethotrexateMechanism of actionAntirheumatic AgentsCytokinesTumor necrosis factor alphaRNA InterferenceApremilastPhosphodiesterase 4 Inhibitorsmedicine.symptomInflammation MediatorsIntracellularMedicamentsmedicine.drugResearch Article
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Is there any place for PD-1/CTLA-4 inhibitors combination in the first-line treatment of advanced NSCLC?—A trial-level meta-analysis in PD-L1 selecte…

2021

BACKGROUND: The advent of immuno-oncology (IO) represented a breakthrough in non-small cell lung cancer (NSCLC) therapy over the last few years. However, establishing the optimal therapeutic options among programmed death-ligand 1 (PD-L1) selected subgroups still addresses an unmet need in the clinical setting. METHODS: We performed a systematic review and finally included eleven first-line randomized controlled trials to compare efficacy and safety outcomes among first-line IO treatment strategies versus standard platinum-based chemotherapy (CT) according to PD-L1 expression level (<1%, 1–49%, ≥50%). Pooled hazard ratios (HRs) and risk ratios (RRs) for progression-free survival (PFS), over…

Oncologymedicine.medical_specialtyprogrammed death-1/cytotoxic T-lymphocyte antigen 4 inhibitors (PD-1/CTLA-4 inhibitors)combined modality therapybusiness.industryHazard ratioCombined modality therapy; Immunotherapy; Meta-analysis; Non-small cell lung cancer (NSCLC); Programmed death-1/cytotoxic T-lymphocyte antigen 4 inhibitors (PD-1/CTLA-4 inhibitors)non-small cell lung cancer (NSCLC)Non-small cell lung cancer (NSCLC)medicine.diseaselaw.inventionDiscontinuationmeta-analysisOncologyRandomized controlled triallawRelative riskInternal medicineMeta-analysisMedicineOriginal ArticleimmunotherapybusinessLung cancerAdverse effect
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Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.

2012

Reactive oxygen species (ROS) are involved in the pathogenesis of many inflammatory diseases such as chronic obstructive pulmonary disease (COPD). They can alter the expression of genes involved in cellular damage by activating transcription factors, including the NF-κB and the activator protein 1 (AP-1). Phosphodiesterase type 4 (PDE4) inhibitors have anti-inflammatory and antioxidant effects, as described in in vivo and in vitro COPD models. This study analysed the effects of piclamilast, a selective PDE4 inhibitor, on modulating the global gene expression profile in A549 cells exposed to H(2)O(2).Changes in gene expression were analysed using high-density Affymetrix microarrays and valid…

Proto-Oncogene Proteins c-junPyridinesActivating transcription factorApoptosisBiologymedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundPulmonary Disease Chronic ObstructiveIn vivoAnnexinCell Line TumorGene expressionmedicineHumansRNA MessengerPhosphorylationCell ProliferationOligonucleotide Array Sequence AnalysisA549 cellGene Expression ProfilingNF-kappa BGeneral MedicineCell Cycle CheckpointsHydrogen PeroxideMolecular biologyTranscription Factor AP-1chemistryGene Expression RegulationAlveolar Epithelial CellsBenzamidesPhosphodiesterase 4 InhibitorsSignal transductionReactive Oxygen SpeciesPiclamilastOxidative stressSignal TransductionFree radical research
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Roflumilast N-oxide inhibits bronchial epithelial to mesenchymal transition induced by cigarette smoke in smokers with COPD.

2014

Abstract Background Epithelial to mesenchymal transition (EMT) is under discussion as a potential mechanism of small airway remodelling in COPD. In bronchial epithelium of COPD and smokers markers of EMT were described. In vitro, EMT may be reproduced by exposing well-differentiated human bronchial epithelial cells (WD-HBEC) to cigarette smoke extract (CSE). EMT may be mitigated by an increase in cellular cAMP. Objective This study explored the effects of roflumilast N-oxide, a PDE4 inhibitor on CSE-induced EMT in WD-HBEC and in primary bronchial epithelial cells from smokers and COPD in vitro. Methods WD-HBEC from normal donors were stimulated with CSE (2.5%) for 72 h in presence of roflum…

Pulmonary and Respiratory MedicineCyclopropanesMalePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionAminopyridinesVimentinApoptosisBronchiEnzyme-Linked Immunosorbent AssayRespiratory MucosaIn Vitro TechniquesTransforming Growth Factor beta1Pulmonary Disease Chronic ObstructiveAnnexinSmokemedicineCyclic AMPHumansPharmacology (medical)Epithelial–mesenchymal transitiontabac efectes fisiològicsRoflumilastAgedchemistry.chemical_classificationReactive oxygen speciesbiologybusiness.industryBiochemistry (medical)Mesenchymal stem cellSmokingNOX4Epithelial CellsfarmacologiaMiddle Agedrespiratory tract diseaseschemistryApoptosisBenzamidesbiology.proteinCancer researchFemalePhosphodiesterase 4 Inhibitorspulmons malalties obstructivesbusinessReactive Oxygen Speciesmedicine.drugPulmonary pharmacologytherapeutics
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Simvastatin Increases the Ability of Roflumilast N-oxide to Inhibit Cigarette Smoke-Induced Epithelial to Mesenchymal Transition in Well-differentiat…

2014

Cigarette smoking contributes to epithelial-mesenchymal transition (EMT) in COPD small bronchi as part of the lung remodeling process. We recently observed that roflumilast N-oxide (RNO), the active metabolite of the PDE4 inhibitor roflumilast, prevents cigarette smoke-induced EMT in differentiated human bronchial epithelial cells. Further, statins were shown to protect renal and alveolar epithelial cells from EMT. To analyze how RNO and simvastatin (SIM) interact on CSE-induced EMT in well-differentiated human bronchial epithelial cells (WD-HBEC) from small bronchi in vitro. Methods: WD-HBEC were stimulated with CSE (2.5%). The mesenchymal markers vimentin, collagen type I and α-SMA, the e…

Pulmonary and Respiratory MedicineCyclopropanesSimvastatinEpithelial-Mesenchymal TransitionAminopyridinesSaludVimentinBronchiPharmacologyMedicineHumansEpithelial–mesenchymal transitionRoflumilastCells Culturedbeta CateninLungbiologybusiness.industryMesenchymal stem cellSmokingEpithelial Cellsrespiratory systemTabaquismoIn vitroBlotTabacomedicine.anatomical_structureSimvastatinBenzamidesbiology.proteinCancer researchPhosphodiesterase 4 InhibitorsHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessReactive Oxygen SpeciesProto-Oncogene Proteins c-aktmedicine.drugCOPD
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Impact of Glucose-Lowering Medications on Cardiovascular and Metabolic Risk in Type 2 Diabetes

2020

Type 2 Diabetes Mellitus (T2DM) is associated with a high risk of atherosclerotic cardiovascular (CV) disease. Among the well-known pathophysiologic factors, crucial roles are played by endothelial dysfunction (caused by oxidative stress and inflammation hyperglycemia-linked), increased activity of nuclear factor kB, altered macrophage polarization, and reduced synthesis of resident endothelial progenitor cells. As consequence, a potentially rapid progression of the atherosclerotic disease with a higher propensity to unstable plaque is arguable, finally leading to significantly increased cardiovascular mortality. Main managements are focused on both prevention and early diagnosis, by target…

cardiovascular riskcardiovascular risk; dipeptidyl peptidase-4 inhibitors; glucagon like peptide-1 receptor agonists; sodium glucose cotransporter-2 inhibitors; type 2 diabetes mellitustype 2 diabetes mellitusglucagon like peptide-1 receptor agonistslcsh:Medicine030209 endocrinology & metabolismInflammationType 2 diabetesDiseaseReview030204 cardiovascular system & hematologyHypoglycemiaBioinformaticsmedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineEndothelial dysfunctionAdverse effectbusiness.industrylcsh:RType 2 Diabetes MellitusGeneral Medicinemedicine.diseasesodium glucose cotransporter-2 inhibitorsmedicine.symptombusinessdipeptidyl peptidase-4 inhibitorsOxidative stressJournal of Clinical Medicine
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Glucose lowering and anti-atherogenic effects of incretin-based therapies: GLP-1 analogues and DPP-4-inhibitors

2009

Type 2 diabetes is a chronic, progressive disease with a multi-faceted pathophysiology. Beyond the known defects of insulin resistance and beta-cell insufficiency, derangement of incretin hormones normally produced from the gut wall in response to food intake play an important role. In recent years, the 'incretin-based' therapies (IBTs) have been developed to address hyperglycemia through either mimicking the action of the endogenous incretin glucagon-like polypeptide (GLP-1) (GLP-1 receptor agonists) or by inhibiting the activity of the enzyme that degrades GLP-1 (the dipeptyl peptidase-4 inhibitors).We reviewed available evidence on the glucose lowering and anti-atherogenic effects of IBT…

endocrine systemmedicine.medical_specialtyDipeptidyl Peptidase 410265 Clinic for Endocrinology and DiabetologyIncretin610 Medicine & healthType 2 diabetesCarbohydrate metabolismIncretinsInsulin resistancecardiovascular risk diabetes DPP-4 inhibitors GLP-1 analoguesGlucagon-Like Peptide 1Risk FactorsInternal medicineDiabetes mellitusmedicineAnimalsHumans2736 Pharmacology (medical)Pharmacology (medical)Dipeptidyl peptidase-4PharmacologyClinical Trials as TopicDipeptidyl-Peptidase IV Inhibitorsbusiness.industrydigestive oral and skin physiologyGeneral MedicineAtherosclerosismedicine.diseaseGlucose3004 PharmacologyEndocrinologyPostprandialDiabetes Mellitus Type 2aterosclerosibusinesshormones hormone substitutes and hormone antagonistsHormoneExpert Opinion on Investigational Drugs
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Future perspectives of the pharmacological management of diabetic dyslipidemia

2019

Introduction: Diabetic dyslipidemia is frequent among patients with type 2 diabetes mellitus (T2DM) and is characterized by an increase in triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C), and small-dense (atherogenic) particles, and by a decrease in low high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (Apo) A1 that are strongly related to insulin resistance. The increased flux of free fatty acids from adipose tissue to the liver aggravates hepatic insulin resistance and promotes all of aspects of the dyslipidemic state. Areas covered: Statins are the first-line agents for treatment while other lipid-lowering drugs (ezetimibe, fibrate and proprotein convertase…

medicine.medical_specialtyApolipoprotein Bmedicine.drug_classglucagon like peptide-1 receptor agonist (GLP-1RA)Fibrate030226 pharmacology & pharmacystatins03 medical and health sciences0302 clinical medicineInsulin resistanceEzetimibeInternal medicinemedicineHumansHypoglycemic AgentsPharmacology (medical)General Pharmacology Toxicology and PharmaceuticsOmega 3 fatty acidDyslipidemiasHypolipidemic Agentsfibratebiologybusiness.industrydyslipidemianutritional and metabolic diseasesType 2 Diabetes MellitusGeneral MedicineLipidmedicine.diseasesodium/glucose cotransporter 2 inhibitors (SGLT-2is)LipidsEndocrinologyDiabetes Mellitus Type 2Cardiovascular Diseases030220 oncology & carcinogenesisDipeptidyl peptidase-4 inhibitors (DPP-4is)Dietary Supplementsbiology.proteinKexinlipids (amino acids peptides and proteins)Hydroxymethylglutaryl-CoA Reductase InhibitorHydroxymethylglutaryl-CoA Reductase InhibitorsInsulin ResistancebusinessDyslipidemiamedicine.drugezetimibeproprotein convertase subtilisin/kexin type 9 (PCSK9)
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Use of Novel Antidiabetic Agents in Patients with Type 2 Diabetes and COVID-19: A Critical Review

2021

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19). The latter is a pandemic that has the potential of developing into a severe illness manifesting as systemic inflammatory response syndrome, acute respiratory distress syndrome, multi-organ involvement and shock. In addition, advanced age and male sex and certain underlying health conditions, like type 2 diabetes mellitus (T2DM), predispose to a higher risk of greater COVID-19 severity and mortality. This calls for an urgent identification of antidiabetic agents associated with more favourable COVID-19 outcomes among patients with T2DM, as well as recognition of their potential underlying…

medicine.medical_specialtyCoronavirus disease 2019 (COVID-19)1 receptor agonists Sodium-glucose co-transporter&nbspEndocrinology Diabetes and MetabolismSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)COVID-19 Dipeptidyl peptidase&nbspReviewType 2 diabetesSodium-glucose co-transporter 2 inhibitorsType 2 diabetesGlucagon-like peptide 1 receptor agonistsDiabetes mellitusPandemicInternal Medicinemedicine2 diabetesIntensive care medicineAntidiabetic agents4 inhibitors Glucagon-like peptide&nbspbusiness.industryCOVID-19medicine.diseaseSystemic inflammatory response syndromeShock (circulatory)Dipeptidyl peptidase 4 inhibitorsmedicine.symptombusiness2 inhibitors Type&nbspDiabetes Therapy
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Phosphodiesterase-4 inhibition improves corticosteroid insensitivity in pulmonary endothelial cells under oxidative stress.

2012

Several clinical studies have shown that smoking in asthmatics and chronic obstructive pulmonary disease patients is closely associated with corticosteroid refractoriness. In this work, we have analyzed glucocorticoid insensitivity in human pulmonary artery endothelial cells (HPAECs) under cigarette smoke extract (CSE) exposure as well as the possible additive effects of the combination therapy with a phosphodiesterase (PDE)-4 inhibitor. Interleukin (IL)-8 was measured in cell supernatants by ELISA. Histone deacetylase (HDAC), histone acetylase (HAT), and intracellular cAMP levels were measured by colorimetric assays and enzyme immunoassay, respectively. PDE4 isotypes and glucocorticoid rec…

medicine.medical_specialtyImmunologyApoptosisDexamethasoneHistone DeacetylasesGlucocorticoid receptorReceptors GlucocorticoidAdrenal Cortex HormonesInternal medicinemedicineCyclic AMPImmunology and AllergyHumansReceptorLungDexamethasoneRolipramCell ProliferationHistone AcetyltransferasesChemistryTumor Necrosis Factor-alphaInterleukin-8InterleukinPhosphodiesteraseEndothelial CellsAparato respiratorioCyclic Nucleotide Phosphodiesterases Type 4Enzyme ActivationOxidative StressEndocrinologyHistone deacetylasePhosphodiesterase 4 InhibitorsPulmonesReactive Oxygen SpeciesRolipramGlucocorticoidmedicine.drugAllergy
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