The effects of pegylated interferon alpha 2b on bile-duct ligation induced liver fibrosis in rats.
OBJECTIVE
To test the effects of peginterferon in an unrecoverable model of bile-duct ligation (BDL) induced liver fibrosis.


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 microgr/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-beta (TGF-beta) levels were examined after four weeks. Liver slides were stained by hematoxylin and eosin and Masson trichrome\Gomory reticulum staining.


RESULTS
The levels of tissue collagen, TGF-beta, 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.
Canbakan
Billur
B
Istanbul University Cerrahpasa Medical Faculty Department of Gastroenterology, Istanbul, Turkey.
Akin
Hakan
H
Tahan
Gulgun
G
Tarcin
Orhan
O
Eren
Fatih
F
Atug
Ozlen
O
Tahan
Veysel
V
Imeryuz
Nese
N
Yapicier
Ozlem
O
Avsar
Erol
E
Tozun
Nurdan
N
D000818:Animals; D001652:Bile Ducts; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology / Q000627:therapeutic use*; D008026:Ligation; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011092:Polyethylene Glycols / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins; D016212:Transforming Growth Factor beta / Q000378:metabolism; D016896:Treatment Outcome
D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D016212:Transforming Growth Factor beta; D011092:Polyethylene Glycols; D008315:Malondialdehyde; D003094:Collagen; C417083:peginterferon alfa-2b; D005978:Glutathione