MARIANA MACIEL TORRES

Índice h a partir de 2011
2
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/07 - Laboratório de Gastroenterologia Clínica e Experimental, Hospital das Clínicas, Faculdade de Medicina

Filtros

Limpar filtros

Configurações

Autor: OLIVEIRA, C. P. ×

Resultados de Busca

Agora exibindo 1 - 3 de 3
  • conferenceObject
    THE COMBINATION OF PROBIOTICS AND PREBIOTICS SUPPLEMENTATION IMPROVES LIPID METABOLISM, NAFLD AND OBESITY IN OB/OB MICE
    (2015) STEFANO, J. T.; TORRES, M. M.; PEREIRA, I. V. A.; JIMENEZ, D.; MUNTANELLI, B.; MALTA, F. M.; COGLIATI, B.; PINHO, J. R. R.; CARRILHO, F. J.; OLIVEIRA, C. P.
  • conferenceObject
    INTRATUMORAL INJECTION OF S-NITROSO-N-ACETYLCYSTEINE (SNAC) IN A RODENT MODEL OF NON-ALCOHOLIC STEATOHEPATITIS (NASH)-RELATED HEPATOCELLULAR CARCINOMA (HCC)
    (2014) STEFANO, J. T.; TORRES, M. M.; PEREIRA, I. V. A.; COGLIATI, B.; OLIVEIRA, M. G. de; CHAMMAS, C.; CARRILHO, F. J.; OLIVEIRA, C. P.
  • article 20 Citação(ões) na Scopus
    Sorafenib prevents liver fibrosis in a non-alcoholic steatohepatitis (NASH) rodent model
    (2015) STEFANO, J. T.; PEREIRA, I. V. A.; TORRES, M. M.; BIDA, P. M.; COELHO, A. M. M.; XERFAN, M. P.; COGLIATI, B.; BARBEIRO, D. F.; MAZO, D. F. C.; KUBRUSLY, M. S.; D'ALBUQUERQUE, L. A. C.; SOUZA, H. P.; CARRILHO, F. J.; OLIVEIRA, C. P.
    Liver fibrosis occurring as an outcome of non-alcoholic steatohepatitis (NASH) can precede the development of cirrhosis. We investigated the effects of sorafenib in preventing liver fibrosis in a rodent model of NASH. Adult Sprague-Dawley rats were fed a choline-deficient high-fat diet and exposed to diethylnitrosamine for 6 weeks. The NASH group (n=10) received vehicle and the sorafenib group (n=10) received 2.5 mg.kg(-1).day(-1) by gavage. A control group (n=4) received only standard diet and vehicle. Following treatment, animals were sacrificed and liver tissue was collected for histologic examination, mRNA isolation, and analysis of mitochondrial function. Genes related to fibrosis (MMP9, TIMP1, TIMP2), oxidative stress (HSP60, HSP90, GST), and mitochondrial biogenesis (PGC1 alpha) were evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Liver mitochondrial oxidation activity was measured by a polarographic method, and cytokines by enzyme-linked immunosorbent assay (ELISA). Sorafenib treatment restored mitochondrial function and reduced collagen deposition by nearly 63% compared to the NASH group. Sorafenib upregulated PGC1 alpha and MMP9 and reduced TIMP1 and TIMP2 mRNA and IL-6 and IL-10 protein expression. There were no differences in HSP60, HSP90 and GST expression. Sorafenib modulated PGC1 alpha expression, improved mitochondrial respiration and prevented collagen deposition. It may, therefore, be useful in the treatment of liver fibrosis in NASH.