DENISE FREDIANI BARBEIRO

(Fonte: Lattes)
Índice h a partir de 2011
15
Lattes
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina

Filtros

Limpar filtros

Configurações

Revista / Livro: Hepatology ×

Resultados de Busca

Agora exibindo 1 - 3 de 3
  • conferenceObject
    Urinary NGAL biomarker predicts non response to therapy with albumin and terlipressin in patients with hepatorenal syndrome
    (2016) XIMENES, Rafael O.; HELOU, Claudia; BARBEIRO, Denise F.; SOUZA, Heraldo; MIGITA, Beatriz; D'ALBUQUERQUE, Luiz C.; CARRILHO, Flair J.; FARIAS, Alberto O.
  • conferenceObject
    Early Predictors of AKI Development/Progression in Patients with Cirrhosis and Ascites Admitted with a Bacterial Infection
    (2018) XIMENES, Rafael Oliveira; HELOU, Claudia Maria B.; SOUZA, Heraldo P.; BARBEIRO, Denise F.; MENDES, Liliana; MARTINELLI, Ana C.; MAZO, Daniel; ALVARES-DA-SILVA, Mario R.; CIARLEGLIO, Maria; DENG, Yanhong; CARRILHO, Flair Jose; GARCIA-TSAO, Guadalupe; FARIAS, Alberto Q.
  • conferenceObject
    Sorafenib improves liver mitochondrial dysfunction attenuating liver fibrosis in non-alcoholic steatohepatitis (NASH) model
    (2012) STEFANO, Jose Tadeu; PEREIRA, Isabel V.; COELHO, Ana Maria M.; XERFAN, Mariana P.; BARBEIRO, Denise F.; TORRES, Mariana Maciel; BIDA, Patricia Martins; MAZO, Daniel F.; COGLIATI, Bruno; SOUZA, Heraldo Possolo; D'ALBUQUERQUE, Luiz C.; CARRILHO, Flair J.; OLIVEIRA, Claudia P.
    Background/Aim: Mitochondria dysfunction in liver may play an important role in the induction of NASH and fibrosis. Recent evidences have shown that kinase inhibitors are able to inhibit angiogenesis, a key mechanism in fibrosis development. We investigated the role of sorafenib as an antifibrotic agent in a rodent model of NASH. Methods: Adult Sprague-Dawley rats, weighing 250-300g, were fed a choline-deficient high fat diet (CDHFD)(35% total fat, 54% trans fatty acid enriched) and simultaneously exposed to diethylnitrosamine (DEN)(100 mg/Kg) in drinking water during 6 weeks to induce NASH and fibrosis. Sorafenib group (n=10) received sorafenib 2.5 mg/kg/day; NASH group (n=10) received CDHFD plus DEN by daily gavage. Control group (n=4) was fed a standard diet. After this period the animals were sacrificed and liver tissues were collected for histologic examination, mRNA isolation and analysis of mitochondrial function. Genes related to fibrosis [matrix metalloproteinases-9 (MMP-9), tissue inhibitor of matrix metalloproteinases 1 and 2 (TIMP-1 and 2)], oxidative stress [Heat Shock Protein 60 and 90 (HSP-60 and 90)] and mitochondrial biogenesis [peroxisome proliferator-activated receptorgamma co-activator 1 α (PGC-1 α )] were evaluated by RT-qPCR method. Liver mitochondrial oxidation and phosphorylation activities were measured by polarographic method. Results: Sorafenib treatment restored the liver mitochondrial function almost similar with control group, and increased RCR and state 3 respiration in comparison to NASH group (Table 1). Besides, sorafenib upregulated PGC-1 α (p<0,001), a gene related to mitochondrial biogenesis. In the other side, TIMP-2 gene expression also was upregulated (p=0,026). There was no difference in expression of HSP-60 (p=0,447), HSP-90 (p=0,141), TIMP-1 (p=0,623) and MMP-9 (p=0,623) between both groups. All of the animals treated with sorafenib showed a significant lost weight and a decreased of fibrosis score in comparison to control (p<0.05). Conclusions: 1) Treatment with sorafenib reduced fibrosis in a rodent model of NASH; 2)Sorafenib increased mRNA expression of PGC-1α and TIMP-2. 3) Sorafenib treatment improves liver mitochondrial dysfunction. Considering that PGC1 α coordinates gene expression that stimulates mitochondrial biogenesis and the TIMP-2 abrogates endothelial cell proliferation and blocks angiogenesis, sorafenib could be used in the treatment of liver fibrosis and prevent fibrosis in this model.