Canbakan B, Akin H,Tahan G, Tarcin O, Eren F, Atug O, Tahan V, Imeryuz N, Yapicier O, Avsar E, Tozun N

Language: English
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Page: 234-240
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ABSTRACT

Objective: To test the effects of peginterferon in an unrecoverable model of bile-duct ligation (BDL) induced liver fibrosis. Material and methods: Thirty-seven Wistar rats were divided into five groups: group 1, BDL + peginterferon (n = 8); group 2, BDL (n = 8); group 3, sham + peginterferon (n = 7); group 4, sham (n = 7); and group 5, control group (n = 7). Peginterferon-alpha 2b (50 µgr/kg) or saline (1 mL/kg) was administered intraperitonealy every week for four weeks. Serum biochemical markers, liver tissue oxidative stress, collagen and transforming growth factor-β (TGF-β) levels were examined after four weeks. Liver slides were stained by hematoxylin and eosin and Masson trichromeGomory reticulum staining. Results: The levels of tissue collagen, TGF-β, biochemical markers (AST, ALT, bilirubins, alkaline phosphates, gamma-glutamyl transpeptidase) and oxidative stress markers (Malondialdehyde, luminal, lucigenin) of the BDL group were higher than the sham operated and control groups (all-p ͑ 0.001). Peginterferon improved malondialdehyde, luminal and glutathione levels in the BDL + peginterferon group (p ‹ 0.05). Histopathological examination of the BDL groups showed stage-3 fibrosis, while all the control groups were normal. Peginterferon showed no improvement in fibrosis either histologically, or biochemically. Conclusions: Peginterferon improved levels of malondialdehyde, glutathione and luminal in the rat model of BDL induced liver fibrosis. Peginterferon however, showed no anti-fibrotic effects in this model and therefore may not be a useful treatment for liver fibrosis.