کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9252835 | 1210876 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The peroxisome proliferator-activated receptor-γ agonist, pioglitazone, inhibits fat accumulation and fibrosis in the livers of rats fed a choline-deficient, l-amino acid-defined diet
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موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Administration of a choline-deficient, l-amino acid-defined (CDAA) diet to rats causes steatohepatitis, hepatic fibrosis, and hepatocellular carcinoma, a pathology similar to that observed in non-alcoholic steatohepatitis (NASH). The aim of this study was to evaluate if a peroxisome proliferator-activated receptor (PPAR)-γ agonist, pioglitazone (PGZ), could ameliorate CDAA diet-induced fatty liver and cirrhosis. Rats were fed a CDAA diet for 1 week and were given the CDAA diet for an additional week with or without PGZ (2-week model). Also, after administration of the CDAA diet for 12 weeks, rats were administered the CDAA diet for an additional 4 weeks with or without PGZ (16-week model). The CDAA diet, administered for either one or 12 weeks, induced fatty liver or cirrhosis with up-regulation of hepatic PPAR-γ expression, respectively. In the 2-week model, rats treated with PGZ for 1 week demonstrated significantly lower hepatic triglyceride content and serum levels of tumor necrosis factor-α. In the 16-week model, treatment for 4 weeks with PGZ ameliorated hepatic fibrosis with a decrease in the expression of procollagen, α-smooth muscle actin, and transforming growth factor-β1 in comparison to rats without PGZ. These results suggest that PPAR-γ agonist is a potential therapeutic modality to treat NASH.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Hepatology Research - Volume 32, Issue 4, August 2005, Pages 235-242
Journal: Hepatology Research - Volume 32, Issue 4, August 2005, Pages 235-242
نویسندگان
Hirofumi Uto, Chihiro Nakanishi, Akio Ido, Satoru Hasuike, Kazunori Kusumoto, Hiroo Abe, Masatsugu Numata, Kenji Nagata, Katsuhiro Hayashi, Hirohito Tsubouchi,