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| OLIVEIRA,MARCOS ROBERTO DE. |
| Vitamin A (retinol) and its congeners - the retinoids - participate in a panoply of biological events, as for instance cell differentiation, proliferation, survival, and death, necessary to maintain tissue homeostasis. Furthermore, such molecules may be applied as therapeutic agents in the case of some diseases, including dermatological disturbances, immunodeficiency, and cancer (mainly leukemia). In spite of this, there is a growing body of evidences showing that vitamin A doses exceeding the nutritional requirements may lead to negative consequences, including bioenergetics state dysfunction, redox impairment, altered cellular signaling, and cell death or proliferation, depending on the cell type. Neurotoxicity has long been demonstrated as a possible... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Mitochondrial dysfunction; Neurotoxicity; Oxidative stress; Retinoids; Vitamin A. |
| Ano: 2015 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652015000301361 |
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| 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... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: NASH; Fibrosis; Mitochondrial dysfunction; Sorafenib. |
| Ano: 2015 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000500408 |
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