Literature DB >> 20969493

Adenovirus-mediated peroxisome proliferator activated receptor gamma overexpression prevents nutritional fibrotic steatohepatitis in mice.

Yue-Min Nan1, Fang Han, Ling-Bo Kong, Su-Xian Zhao, Rong-Qi Wang, Wen-Juan Wu, Jun Yu.   

Abstract

OBJECTIVE: The pathogenesis of non-alcoholic steatohepatitis is still unclear. We have demonstrated previously that peroxisome proliferator activated receptor gamma (PPARγ) ligand protects against inflammation and fibrogenesis in experimental non-alcoholic steatohepatitis. We aim to elucidate the effect and the mechanism of PPARγ itself on nutritional fibrotic steatohepatitis in mice.
METHODS: C57BL/6J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrotic steatohepatitis. Mice fed the MCD diet were treated with adenovirus carrying PPARγ (Ad-PPARγ), Ad-PPARγ plus PPARγ agonist rosiglitazone, or PPARγ antagonist 2-chloro-5-nitrobenzaniliden (GW9662), respectively. The effects of up-regulation of PPARγ in the presence or absence of its agonist/or antagonist were assessed by comparing the severity of hepatic injury, activation of hepatic stellate cells and the expression of adiponectin, heme oxygenase-1, and fibrogenic related genes.
RESULTS: Mice fed with MCD diet for 8 weeks showed severe hepatic injury including hepatic steatosis, inflammatory infiltration, and fibrosis. Administration of Ad-PPARγ significantly lowered serum alanine aminotransferase level and ameliorated hepatic steatosis, necroinflammation, and fibrosis. These effects were associated with enhanced expression of PPARγ, up-regulated expression of adiponectin and heme oxygenase-1, and down-regulated expression of tumor necrosis factor alpha, interleukin-6, α-smooth muscle actin, transforming growth factor beta 1, matrix metallopeptidase-2, and -9. Administration of GW9662 promoted the severity of liver histology.
CONCLUSIONS: The present study provided evidences for the protective role of overexpressing PPARγ in ameliorating hepatic fibrosing steatohepatitis in mice. Modulation of PPARγ expression might serve as a therapeutic approach for fibrotic steatohepatitis.

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Year:  2010        PMID: 20969493     DOI: 10.3109/00365521.2010.525717

Source DB:  PubMed          Journal:  Scand J Gastroenterol        ISSN: 0036-5521            Impact factor:   2.423


  28 in total

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8.  Methionine-restricted C57BL/6J mice are resistant to diet-induced obesity and insulin resistance but have low bone density.

Authors:  Gene P Ables; Carmen E Perrone; David Orentreich; Norman Orentreich
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9.  The Current Knowledge of the Role of PPAR in Hepatic Ischemia-Reperfusion Injury.

Authors:  M Elias-Miró; M B Jiménez-Castro; M Mendes-Braz; A Casillas-Ramírez; C Peralta
Journal:  PPAR Res       Date:  2012-05-16       Impact factor: 4.964

10.  Update on pparγ and nonalcoholic Fatty liver disease.

Authors:  Gene P Ables
Journal:  PPAR Res       Date:  2012-08-16       Impact factor: 4.964

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