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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

S-nitroso-N-acetylcysteine attenuates liver fibrosis in experimental nonalcoholic steatohepatitis

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Mazo, Daniel F. C. [1] ; de Oliveira, Marcelo G. [2] ; Pereira, Isabel V. A. [1] ; Cogliati, Bruno [3] ; Stefano, Jose T. [1] ; de Souza, Gabriela F. P. [2] ; Rabelo, Fabiola [1] ; Lima, Fabiana R. [4] ; Alves, Venancio A. Ferreira [4] ; Carrilho, Flair J. [1] ; de Oliveira, Claudia P. M. S. [1]
Total Authors: 11
[1] Univ Sao Paulo, Sch Med, Dept Gastroenterol, Hepatol Branch LIM 07, Clin Div, Sao Paulo - Brazil
[2] Univ Estadual Campinas, UNICAMP, Inst Chem, BR-13083970 Campinas, SP - Brazil
[3] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, Sao Paulo - Brazil
[4] Univ Sao Paulo, Sch Med, Dept Pathol LIMI4, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: DRUG DESIGN DEVELOPMENT AND THERAPY; v. 7, p. 553-563, 2013.
Web of Science Citations: 14

S-Nitroso-N-acetylcysteine (SNAC) is a water soluble primary S-nitrosothiol capable of transferring and releasing nitric oxide and inducing several biochemical activities, including modulation of hepatic stellate cell activation. In this study, we evaluated the antifibrotic activity of SNAC in an animal model of nonalcoholic steatohepatitis (NASH) induced in Sprague-Dawley rats fed with a choline-deficient, high trans fat diet and exposed to diethylnitrosamine for 8 weeks. The rats were divided into three groups: SNAC, which received oral SNAC solution daily; NASH, which received the vehicle; and control, which received standard diet and vehicle. Genes related to fibrosis (matrix metalloproteinases {[}MMP]-13, -9, and -2), transforming growth factor beta-1 {[}TGF beta-1], collagen-1 alpha, and tissue inhibitors of metalloproteinase {[}TIMP-1 and -2] and oxidative stress (heat-shock proteins {[}HSP]-60 and -90) were evaluated. SNAC led to a 34.4% reduction in the collagen occupied area associated with upregulation of MMP-13 and -9 and downregulation of HSP-60, TIMP-2, TGF beta-1, and collagen-1 alpha. These results indicate that oral SNAC administration may represent a potential antifibrotic treatment for NASH. (AU)