الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 166 |  |  |
| | | from | 166 | | |
Abstract
Despite the progress in hepatology, hepatic fibrosis still remains a major cause of morbidity and mortality globally. The current study aimed to investigate the potential antifibrotic effects of dimethylfumarate (DMF) on liver fibrosis induced by carbon tetrachloride (CCl4) or thioacetamide (TAA) in rats. Biochemical and histopathological changes were assessed, including: Liver function tests. Oxidative stress-related parameters. Inflammation and fibrosis biomarkers. Histopathology and immunohistochemistry. Interestingly, the antifibrotic effects of DMF were more pronounced in the 8-week groups in both models, reflecting that the reversibility of fibrosis by DMF may decline with prolonged exposure to CCl4 or TAA, and/or delayed initiation of the treatment with DMF. Dimethylfumarate possesses hepatoprotective and antifibrotic properties against liver injury and fibrosis induced by both CCl4 and TAA. These effects could be attributed to amelioration of antioxidant status as well as modulation of inflammatory and fibrotic cascades. The antifibrotic potential of DMF may be decreased with delayed initiation and/or prolonged duration of exposure to CCl4 or TAA. Further clinical studies are required to confirm these experimental effects in patients at risk of developing hepatic injury and fibrosis.