Abstract | BACKGROUND: AIMS: To evaluate if pirfenidone maintains its anti-fibrotic properties also when administered after the induction of hepatic damage and to further investigate the molecular mechanisms leading to the anti-fibrotic effect of pirfenidone. METHODS AND RESULTS: CONCLUSIONS: (1) Pirfenidone is effective also if administered after the induction of the hepatic damage; (2) the anti-fibrotic effect of pirfenidone is mainly due to the reduced expression of profibrogenic procollagen alpha1(I) and TIMP-1, most likely through the downregulation of transforming growth factorbeta1 mRNA, and of matrix metalloproteinase-2, which is mainly implicated in the degradation of the normal extracellular matrix.
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Authors | A Di Sario, E Bendia, G Macarri, C Candelaresi, S Taffetani, M Marzioni, A Omenetti, S De Minicis, L Trozzi, A Benedetti |
Journal | Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
(Dig Liver Dis)
Vol. 36
Issue 11
Pg. 744-51
(Nov 2004)
ISSN: 1590-8658 [Print] Netherlands |
PMID | 15571005
(Publication Type: Journal Article)
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Chemical References |
- Collagen Type I
- Pyridones
- Tissue Inhibitor of Metalloproteinase-1
- pirfenidone
- Matrix Metalloproteinase 2
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Topics |
- Animals
- Collagen Type I
(physiology)
- Down-Regulation
- Liver Cirrhosis
(drug therapy, physiopathology)
- Male
- Matrix Metalloproteinase 2
(physiology)
- Pyridones
(therapeutic use)
- Rats
- Rats, Sprague-Dawley
- Tissue Inhibitor of Metalloproteinase-1
(physiology)
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