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| 1 | Chronic exposure to ethanol causes steatosis and inflammation in zebrafish liver显示文摘AIM To evaluate the effects of chronic exposure to ethanol in the liver and the expression of inflammatory genesin zebrafish.METHODS Zebrafish(n = 104),wild type,adult,male and female,were divided into two groups:Control and ethanol(0.05 v/v).The ethanol was directly added into water;tanks water were changed every two days and the ethanol replaced.The animals were fed twice a day with fish food until satiety.After two and four weeks of trial,livers were dissected,histological analysis(hematoxilineosin and Oil Red staining) and gene expression assessment of adiponectin,adiponectin receptor 2(adipor2),sirtuin-1(sirt-1),tumor necrosis factor-alpha(tnf-a),interleukin-1b(il-1b) and interleukin-10(il-10) were performed.Ultrastructural evaluations were conducted at fourth week.RESULTS Exposing zebrafish to 0.5% ethanol developed intense liver steatosis after four weeks,as demonstrated by oil red staining.In ethanol-treated animals,the main ultrastructural changes were related to cytoplasmic lipid particles and droplets,increased number of rough endoplasmic reticulum cisterns and glycogen particles.Between two and four weeks,hepatic mR NA expression of il-1b,sirt-1 and adipor2 were upregulated,indicating that ethanol triggered signaling molecules which are key elements in both hepatic inflammatory and protective responses.Adiponectin was not detected in the liver of animals exposed and not exposed to ethanol,and il-10 did not show significant difference.CONCLUSION Data suggest that inflammatory signaling and ultrastructural alterations play a significant role during hepatic steatosis in zebrafish chronically exposed to ethanol. | Ana Claudia Reis Schneider Cleandra Gregório Carolina Uribe-Cruz Ranieli Guizzo Tais Malysz Maria Cristina Faccioni-Heuser Larisse Longo Themis Reverbel da Silveira | 2017 | World Journal of Hepatology2017，9，8： | 7 |
| 2 | Hepatocellular carcinoma staging systems: Hong Kong liver cancer vs Barcelona clinic liver cancer in a Western population显示文摘BACKGROUND Despite being the world’s most widely used system for staging and therapeutic guidance in hepatocellular carcinoma(HCC)treatment,the Barcelona clinic liver cancer(BCLC)system has limitations,especially regarding intermediate-grade(BCLC-B)tumors.The recently proposed Hong Kong liver cancer(HKLC)staging system appears useful but requires validation in Western populations.AIM To evaluate the agreement between BCLC and HKLC staging on the management of HCC in a Western population,estimating the overall patient survival.METHODS This was a retrospective study of HCC patients treated at a university hospital in southern Brazil between 2011 and 2016.Demographic,clinical,and laboratory data were collected.HCC staging was carried out according to the HKLC and BCLC systems to assess treatment agreement.Overall survival was estimated based on the treatment proposed in each system.RESULTS A total of 519 HCC patients were assessed.Of these,178(34.3%)were HKLC-I;95(18.3%)HKLC-IIA;47(9.1%)HKLC-IIB;29(5.6%)HKLC-IIIA;30(5.8%)HKLCIIIB;75(14.4%)HKLC-IV;and 65(12.5%)HKLC-V.According to the BCLC,25(4.9%)were BCLC-0;246(47.4%)BCLC-A;107(20.6%)BCLC-B;76(14.6%)BCLCC;and 65(12.5%)BCLC-D.The general agreement between the two systems was 80.0%-BCLC-0 and HKLC-I(100%);BCLC-A and HKLC-I/HKLC-II(96.7%);BCLC-B and HKLC-III(46.7%);BCLC-C and HKLC-IV(98.7%);BCLC-D and HKLC-V(41.5%).When sub-classifying BCLC-A,HKLC-IIB,HKLC-IIIA and HKLC-IIIB stages according to the up-to-7 in/out criterion,13.4,66.0,100 and 36.7%,respectively,of the cases were classified as up-to-7 out.CONCLUSION In a Western population,the general agreement between the two systems was 80.0%,although in BCLC-B cases the agreement was low,suggesting that some individuals could be candidates for the curative treatment recommended by the HKLC.The authors suggest that the BCLC system should be routinely employed,although for BCLC-B cases it should be associated with the HKLC system. | Laura Bainy Rodrigues de Freitas Larisse Longo Deivid Santos Ivana Grivicich Mário Reis Alvares-da-Silva | 2019 | World Journal of Hepatology2019，11，9： | 3 |
| 3 | Gut dysbiosis and systemic inflammation promote cardiomyocyte abnormalities in an experimental model of steatohepatitis显示文摘BACKGROUND Cardiovascular disease is the main cause of death in metabolic-associated fatty liver disease,and gut microbiota dysbiosis is associated with both of them.AIM To assess the relationship between gut dysbiosis and cardiovascular risk(CVR)in an experimental model of steatohepatitis.METHODS Adult male Sprague-Dawley rats were randomized to a control group(n=10)fed a standard diet and an intervention group(n=10)fed a high-fat choline-deficient diet for 16 wk.Biochemical,molecular,hepatic,and cardiac histopathology.Gut microbiota variables were evaluated.RESULTS The intervention group had a significantly higher atherogenic coefficient,Castelli’s risk index(CRI)-I and CRI-II,interleukin-1β,tissue inhibitor of metalloproteinase-1(all P<0.001),monocyte chemoattractant protein-1(P=0.005),and plasminogen activator inhibitor-1(P=0.037)than the control group.Gene expression of miR-33a increased(P=0.001)and miR-126(P<0.001)decreased in the intervention group.Steatohepatitis with fibrosis was seen in the intervention group,and heart computerized histological imaging analysis showed a significant decrease in the percentage of cardiomyocytes with a normal morphometric appearance(P=0.007),reduction in the mean area of cardiomyocytes(P=0.037),and an increase of atrophic cardiomyocytes(P=0.007).There were significant correlations between the cardiomyocyte morphometry markers and those of progression and severity of liver disease and CVR.The intervention group had a lower Shannon diversity index and fewer changes in the structural pattern of gut microbiota(both P<0.001)than controls.Nine microbial families that are involved in lipid metabolism were differentially abundant in intervention group and were significantly correlated with markers of liver injury and CVR.CONCLUSION The study found a link between gut dysbiosis and significant cardiomyocyte abnormalities in animals with steatohepatitis. | Larisse Longo Pabulo Henrique Rampelotto Eduardo Filippi-Chiela Valessa Emanoele Gabriel de Souza Fernando Salvati Carlos Thadeu Cerski Themis Reverbel da Silveira Cláudia P Oliveira Carolina Uribe-Cruz Mário ReisÁlvares-da-Silva | 2021 | World Journal of Hepatology2021，13，12： | 1 |
| 4 | Rifaximin on epigenetics and autophagy in animal model of hepatocellular carcinoma secondary to metabolic-dysfunction associated steatotic liver disease显示文摘BACKGROUND Prevalence of hepatocellular carcinoma(HCC)is increasing,especially in patients with metabolic dysfunctionassociated steatotic liver disease(MASLD).AIM To investigate rifaximin(RIF)effects on epigenetic/autophagy markers in animals.METHODS Adult Sprague-Dawley rats were randomly assigned(n=8,each)and treated from 5-16 wk:Control[standard diet,water plus gavage with vehicle(Veh)],HCC[high-fat choline deficient diet(HFCD),diethylnitrosamine(DEN)in drinking water and Veh gavage],and RIF[HFCD,DEN and RIF(50 mg/kg/d)gavage].Gene expression of epigenetic/autophagy markers and circulating miRNAs were obtained.RESULTS All HCC and RIF animals developed metabolic-dysfunction associated steatohepatitis fibrosis,and cirrhosis,but three RIF-group did not develop HCC.Comparing animals who developed HCC with those who did not,miR-122,miR-34a,tubulin alpha-1c(Tuba-1c),metalloproteinases-2(Mmp2),and metalloproteinases-9(Mmp9)were significantly higher in the HCC-group.The opposite occurred with Becn1,coactivator associated arginine methyltransferase-1(Carm1),enhancer of zeste homolog-2(Ezh2),autophagy-related factor LC3A/B(Map1 Lc3b),and p62/sequestosome-1(p62/SQSTM1)-protein.Comparing with controls,Map1 Lc3b,Becn1 and Ezh2 were lower in HCC and RIF-groups(P<0.05).Carm1 was lower in HCC compared to RIF(P<0.05).Hepatic expression of Mmp9 was higher in HCC in relation to the control;the opposite was observed for p62/Sqstm1(P<0.05).Expression of p62/SQSTM1 protein was lower in the RIF-group compared to the control(P=0.024).There was no difference among groups for Tuba-1c,Aldolase-B,alpha-fetoprotein,and Mmp2(P>0.05).miR-122 was higher in HCC,and miR-34a in RIF compared to controls(P<0.05).miR-26b was lower in HCC compared to RIF,and the inverse was observed for miR-224(P<0.05).There was no difference among groups regarding miR-33a,miR-143,miR-155,miR-375 and miR-21(P>0.05).CONCLUSION RIF might have a possible beneficial effect on preventing/delaying liver carcinogenesis through epigenetic modulation in a rat model of MASLD-HCC. | Matheus Truccolo Michalczuk Larisse Longo Melina Belén Keingeski Bruno de Souza Basso Gabriel Tayguara Silveira Guerreiro Jessica T Ferrari JoséEduardo Vargas Cláudia P Oliveira Carolina Uribe-Cruz Carlos Thadeu Schmidt Cerski Eduardo Filippi-Chiela Mário ReisÁlvares-da-Silva | 2024 | World Journal of Hepatology2024，16，1： | 0 |
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