0000000000301219

AUTHOR

Federico Salomone

0000-0001-5264-2935

showing 7 related works from this author

Hepatitis C virus eradication by direct antiviral agents abates oxidative stress in patients with advanced liver fibrosis

2020

Background and aims: HCV eradication improves non-hepatic outcomes such as cardiovascular diseases, although without clearly defined mechanisms. In this study we aimed to assess whether improvement of carotid atherosclerosis may be linked to a reduction in systemic oxidative stress after viral clearance. Methods: We studied a retrospective cohort of 105 patients (age 62.4 ± 11.2 years; 62 men) with F3/F4 fibrosis, characterized by carotid ultrasonography at baseline and at sustained virologic response (SVR) follow-up. Levels of 8-iso-prostaglandin F2α (F2-isoprostanes) and other oxidative stress markers were measured on frozen sera. Association between change (denoted as Δ) in oxidative str…

Liver CirrhosisMalemedicine.medical_specialtyCirrhosisHepatitis C virus2-isoprostanesHepacivirusmedicine.disease_causeAntiviral AgentsCarotid Intima-Media ThicknessGastroenterology03 medical and health sciencesLiver disease0302 clinical medicineatherosclerosiFFibrosisSettore BIO/13 - Biologia ApplicataInternal medicinemedicineHumansintima-media thicknessAgedRetrospective StudiesSettore MED/12 - GastroenterologiaHepatologybusiness.industrycirrhosisCarotid ultrasonographylipid peroxidationMiddle Agedmedicine.diseaseHepatitis CIsoprostanesatherosclerosis; cirrhosis; F; 2; -isoprostanes; intima-media thickness; lipid peroxidationOxidative StressIntima-media thickness030220 oncology & carcinogenesis030211 gastroenterology & hepatologyatherosclerosisbusinessOxidative stresscirrhosi
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Silibinin modulates lipid homeostasis and inhibits nuclear factor kappa B activation in experimental nonalcoholic steatohepatitis.

2012

Nonalcoholic steatohepatitis (NASH) is associated with increased liver-related mortality. Disturbances in hepatic lipid homeostasis trigger oxidative stress and inflammation (ie, lipotoxicity), leading to the progression of NASH. This study aimed at identifying whether silibinin may influence the molecular events of lipotoxicity in a mouse model of NASH. Eight-week-old db/db mice were fed a methionine-choline deficient (MCD) diet for 4 weeks and treated daily with silibinin (20 mg/kg intraperitoneally) or vehicle. Liver expression and enzyme activity of stearoyl-CoA desaturase-1 and acyl-CoA oxidase, and expression of liver fatty acid-binding protein were assessed. Hepatic levels of reactiv…

Malemedicine.medical_specialtyMice ObeseSilibininmedicine.disease_causeAntioxidantsTranslational Research BiomedicalMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseasePhysiology (medical)Internal medicineNonalcoholic fatty liver diseasemedicineTBARSAnimalsHomeostasisNASH MCD Silibinin lipotoxicity.Reactive nitrogen speciesLiver injurychemistry.chemical_classificationReactive oxygen speciesAnti-Inflammatory Agents Non-SteroidalBiochemistry (medical)NF-kappa BPublic Health Environmental and Occupational HealthGeneral MedicineLipid Metabolismmedicine.diseaseCholine DeficiencyFatty LiverDisease Models AnimalOxidative StressEndocrinologyLiverchemistryLipotoxicitySilybinOxidative stressSilymarin
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Effects of IL28B rs12979860 CC Genotype on Metabolic Profile and Sustained Virologic Response in Patients With Genotype 1 Chronic Hepatitis C

2013

Patients with genotype 1 chronic hepatitis C (G1 CHC) frequently develop steatosis and insulin resistance (IR), caused by metabolic and viral factors. These accelerate the progression of liver disease and reduce the response to therapy. A sustained virologic response (SVR) to therapy in patients with G1 CHC is associated strongly with polymorphisms near the interleukin-28B (IL28B) gene, but the interaction between IL28B genotype and IR, and their combined effects on SVR, have not been defined. We tested the association between the IL28B rs12979860 single-nucleotide polymorphism and metabolic features, including IR, and evaluated their effects on SVR.We performed genotype analysis of IL28B r…

AdultMalemedicine.medical_specialtyGenotypeHepacivirusHepatitis C virusSingle-nucleotide polymorphismHepacivirusmedicine.disease_causeAntiviral AgentsPolymorphism Single NucleotideGastroenterologyCohort StudiesLiver diseaseInsulin resistanceInternal medicineGenotypemedicineHumansAgedinsulin resistance steatosis interleukin-28B sustained virologic responseHepatologybiologybusiness.industryInterleukinsGastroenterologyHepatitis C ChronicMiddle AgedViral Loadmedicine.diseasebiology.organism_classificationTreatment OutcomeInterleukin 28BImmunologyMetabolomeRNA ViralFemaleInterferonsInsulin ResistanceSteatosisbusinessClinical Gastroenterology and Hepatology
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Corrigendum to “Silibinin improves hepatic and myocardial injury in mice with nonalcoholic steatohepatitis” [Dig. Liver Dis. 44 (2012) 334–342]

2012

Nonalcoholic steatohepatitismedicine.medical_specialtyPathologyHepatologybusiness.industryGastroenterologySilibininGastroenterologychemistry.chemical_compoundchemistryInternal medicineDigMedicinebusinessDigestive and Liver Disease
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Silibinin improves hepatic and myocardial injury in mice with nonalcoholic steatohepatitis

2012

Abstract Background Nonalcoholic fatty liver disease is a chronic metabolic disorder with significant impact on cardiovascular and liver mortality. Aims In this study, we examined the effects of silibinin on liver and myocardium injury in an experimental model of nonalcoholic fatty liver disease. Methods A four-week daily dose of silibinin (20 mg/kg i.p.) was administrated to db/db mice fed a methionine–choline deficient diet. Hepatic and myocardial histology, oxidative stress and inflammatory cytokines were evaluated. Results Silibinin administration decreased HOMA-IR, serum ALT and markedly improved hepatic and myocardial damage. Silibinin reduced isoprostanes, 8-deoxyguanosine and nitrit…

MaleGene ExpressionIsoprostanesmedicine.disease_causeGastroenterologyAntioxidantsMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseasePhosphorylationGastroenterologyAlanine TransaminaseGlutathioneCholine DeficiencyMitochondrial respiratory chainLiverHeart Inflammation NAFLD Oxidative stress SilibininCytokinesmedicine.symptomSilymarinmedicine.medical_specialtySilibininInflammationStatistics NonparametricProinflammatory cytokineInsulin resistanceInternal medicinemedicineAnimalsNitritesAnalysis of VarianceNitratesHepatologySettore BIO/16 - Anatomia Umanabusiness.industryMyocardiumJNK Mitogen-Activated Protein KinasesGlutathionemedicine.diseaseDietFatty LiverOxidative StressEndocrinologychemistrySilybinInsulin ResistancebusinessOxidative stressDigestive and Liver Disease
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Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD

2021

Background and aim: Coffee intake exerts protective effects against non-alcoholic fatty liver disease (NAFLD), although without fully cleared mechanisms. In this study we aimed to assess whether coffee consumption may influence the expression of long non-coding RNAs (lncRNAs) in the liver. Methods: C57BL/6J mice were fed a 12-week standard diet (SD), high-fat diet (HFD) or HFD plus decaffeinated coffee solution (HFD + coffee). Expression of specific lncRNAs involved in NAFLD was analyzed by real-time PCR. For the most differentially expressed lncRNAs, the analysis was also extended to their mRNA targets. Results: Decaffeinated coffee intake reduced body weight gain, prevented NAFLD, lowered…

lncRNA.Liver CirrhosisMalemedicine.medical_specialtyGm16551; H19; NAFLD; coffee; lncRNA; Animals; Coffee; Disease Models Animal; Fatty Liver; Gene Expression; Liver; Liver Cirrhosis; Male; Mice; Mice Inbred C57BL; Non-alcoholic Fatty Liver Disease; RNA Long NoncodingCoenzyme ACircadian clockcoffeeGene ExpressionBiologyInbred C57BLArticlechemistry.chemical_compoundMicelncRNADownregulation and upregulationFibrosisSettore BIO/13 - Biologia ApplicataNon-alcoholic Fatty Liver DiseaseInternal medicineNAFLDmedicineAnimalsTX341-641Messenger RNANutrition and DieteticsH19Nutrition. Foods and food supplyAnimalGm16551Fatty liverNAFLD; coffee; lncRNA; Gm16551; H19nutritional and metabolic diseasesmedicine.diseaseMice Inbred C57BLFatty LiverDisease Models AnimalEndocrinologychemistryLiverLipogenesisDisease ModelsRNARNA Long NoncodingLong NoncodingSteatosisFood Science
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Non-Invasive Assessment of Liver Injury in Non-Alcoholic Fatty Liver Disease: A Review of Literature.

2016

NAFLD (Non-Alcoholic Fatty Liver Disease) is an increasingly significant public health issue, regarded as the most relevant liver disease of the twenty-first century. Approximately 20%-30% of NAFLD subjects develop a NASH (Non-Alcoholic Steato-Hepatitis), a condition which can potentially evolve to liver cirrhosis and hepatocellular carcinoma. For these reasons a proper evaluation of liver damage is a key point for diagnosis and prognosis and liver biopsy still remains the "gold standard" procedure both for discrimination between steatosis and steatohepatitis and assessment of the degree of liver fibrosis. Nonetheless, given it is an invasive, painful and costly procedure, a great research …

medicine.medical_specialtyCirrhosisFibrosiBiopsyClinical Decision-MakingApoptosis030204 cardiovascular system & hematologyBiochemistryGastroenterologyMultimodal Imaging03 medical and health sciencesLiver disease0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInternal medicineMedicineAnimalsHumansMortalityMolecular BiologyLiver injurymedicine.diagnostic_testAnimalbusiness.industryFatty liverApoptosiBiomarkerGeneral Medicinemedicine.diseasePrognosisFibrosisdigestive system diseasesAlgorithmLiverLiver biopsyHepatocellular carcinomaMolecular Medicine030211 gastroenterology & hepatologySteatosisSteatohepatitisMorbiditybusinessAlgorithmsBiomarkersHumanCurrent molecular medicine
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