Literature DB >> 16935387

Hepatic gene expression profile associated with non-alcoholic steatohepatitis protection by S-nitroso-N-acetylcysteine in ob/ob mice.

Claudia Pinto Marques Souza de Oliveira1, José Tadeu Stefano, Vicência Mara Rodrigues de Lima, Sandra Valéria de Sá, Fernanda Ibanez Simplicio, Evandro Sobrosa de Mello, Maria Lúcia Corrêa-Giannella, Venâncio Avancini Ferreira Alves, Francisco Rafael Martins Laurindo, Marcelo Ganzarolli de Oliveira, Daniel Giannella-Neto, Flair José Carrilho.   

Abstract

BACKGROUND/AIMS: To understand the molecular mechanisms underlying non-alcoholic steatohepatitis (NASH) prevention by S-nitroso-N-acetylcysteine (SNAC), an NO donor that inhibits lipid peroxidation, we examined hepatic differentially expressed genes between ob/ob mice receiving or not SNAC treatment concomitantly with a methionine-choline deficient (MCD) diet.
METHODS: Ob/ob mice were assigned to receive oral SNAC fed solution (MCD+SNAC group) or vehicle (MCD group) by gavage. After four weeks, histopathological analysis and microarray hybridizations were conducted in liver tissues from groups. GeneSifter system was used to identify differentially expressed genes and pathways according to Gene Ontology.
RESULTS: NASH was absent in the MCD+SNAC group and no significant changes in food intake or body weight were observed in comparison to MCD group. After SNAC treatment, several genes belonging to oxidative phosphorylation, fatty acid biosynthesis, fatty acid metabolism and glutathione metabolism pathways were down-regulated in comparison to the MCD group.
CONCLUSIONS: SNAC treatment promotes down regulation of several genes from fatty acid (FA) metabolism related pathways, possibly through abrogation of the cytotoxic effects of reactive oxygen species and lipid peroxides with consequent prevention of mitochondrial overload. Further studies are required to investigate the clinical implications of these findings, in attempt to develop novel therapeutic strategies for NAFLD treatment.

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Year:  2006        PMID: 16935387     DOI: 10.1016/j.jhep.2006.05.017

Source DB:  PubMed          Journal:  J Hepatol        ISSN: 0168-8278            Impact factor:   25.083


  7 in total

1.  Transcriptional profile of genes involved in oxidative stress and antioxidant defense in a dietary murine model of steatohepatitis.

Authors:  Agnieszka Gornicka; Gareth Morris-Stiff; Samjhana Thapaliya; Bettina G Papouchado; Michael Berk; Ariel E Feldstein
Journal:  Antioxid Redox Signal       Date:  2011-05-05       Impact factor: 8.401

2.  S-nitroso-N-acetylcysteine attenuates liver fibrosis in cirrhotic rats.

Authors:  Rafael Vercelino; Irene Crespo; Gabriela F P de Souza; Maria Jose Cuevas; Marcelo G de Oliveira; Norma Possa Marroni; Javier González-Gallego; María Jesús Tuñón
Journal:  J Mol Med (Berl)       Date:  2010-01-09       Impact factor: 4.599

Review 3.  Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases.

Authors:  Sudheer K Mantena; Adrienne L King; Kelly K Andringa; Heather B Eccleston; Shannon M Bailey
Journal:  Free Radic Biol Med       Date:  2008-01-03       Impact factor: 7.376

4.  S-nitroso-N-acetylcysteine ameliorates ischemia-reperfusion injury in the steatotic liver.

Authors:  Wellington Andraus; Gabriela Freitas Pereira de Souza; Marcelo Ganzarolli de Oliveira; Luciana B P Haddad; Ana Maria M Coelho; Flavio Henrique Galvão; Regina Maria Cubero Leitão; Luiz Augusto Carneiro D'Albuquerque; Marcel Cerqueira Cesar Machado
Journal:  Clinics (Sao Paulo)       Date:  2010-07       Impact factor: 2.365

5.  Long term N-acetylcysteine administration rescues liver steatosis via endoplasmic reticulum stress with unfolded protein response in mice.

Authors:  Ching-Chou Tsai; Yu-Jen Chen; Hong-Ren Yu; Li-Tung Huang; You-Lin Tain; I-Chun Lin; Jiunn-Ming Sheen; Pei-Wen Wang; Mao-Meng Tiao
Journal:  Lipids Health Dis       Date:  2020-05-25       Impact factor: 3.876

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

Authors:  Daniel F C Mazo; Marcelo G de Oliveira; Isabel V A Pereira; Bruno Cogliati; José T Stefano; Gabriela F P de Souza; Fabíola Rabelo; Fabiana R Lima; Venâncio A Ferreira Alves; Flair J Carrilho; Claudia P M S de Oliveira
Journal:  Drug Des Devel Ther       Date:  2013-06-28       Impact factor: 4.162

7.  HbA1c may contribute to the development of non-alcoholic fatty liver disease even at normal-range levels.

Authors:  Changxi Chen; Zhongwei Zhu; Yushan Mao; Yimin Xu; Juan Du; Xiaoping Tang; Hongbao Cao
Journal:  Biosci Rep       Date:  2020-01-31       Impact factor: 3.840

  7 in total

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