N-Acetylcysteine Attenuates Progression of Liver Pathology in a Rat Model of Nonalcoholic Steatohepatitis  

Oleh:

Baumgardne, January N. ; Shankar, Kartik ; Hennings, Leah ; Albano, Emanuele ; Badger, Thomas M. ; Ronis, Martin J. J.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 138 no. 10 (Oct. 2008), page 1872.
Topik: Biochemical; Molecular; and Genetic mechanisms

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2008.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

A "2-hit" model for nonalcoholic steatohepatitis (NASH) has been proposed in which steatosis constitutes the "first hit" and sensitizes the liver to potential "second hits" resulting in NASH. Oxidative stress is considered a candidate for the second hit. N-acetylcysteine (NAC), an antioxidant, has been suggested as a dietary therapy for NASH. We examined the effects of NAC in a rat total enteral nutrition (TEN) model where NASH develops as the result of overfeeding dietary polyunsaturated fat. Male Sprague-Dawley rats consumed pelleted AIN-93G diets ad libitum or were overfed a 9200 kJ·kg–0.75·d–1 liquid diet containing 70% corn oil with or without 2 g·kg–1·d–1 NAC i.g. for 65 d. Hepatic steatosis was not influenced by dietary supplementation with NAC; however, the liver pathology score was lower (P = 0.05) and NAC provided partial protection against alanine aminotransferase release (P = 0.05). NAC attenuated increased hepatic oxidative stress (TBARS; P = 0.05) and prevented increases in cytochrome P450 2E1 apoprotein and mRNA and in tumor necrosis factor-{alpha} (TNF{alpha}) mRNA. Titers of auto-antibodies against proteins adducted to lipid peroxidation products were lower in serum of the NAC group than in the 70% corn oil group (P = 0.05). NAC also decreased Picosirius red staining of collagen, a marker of fibrosis. However, markers of hepatic stellate cell activation were unaffected. Using NAC in a TEN model of NASH, we have demonstrated that NAC prevents many aspects of NASH progression by decreasing development of oxidative stress and subsequent increases in TNF{alpha} but does not block development of steatosis.

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