The aim of the present study was to investigate the effects of
octreotide treatment on hepatic
heme oxygenase-1 (HO-1) expression, together with the influence of altered hepatic HO-1 expression levels on hepatic function and
fibrosis in bile duct-ligated rats. The rats were divided randomly into
sham, cirrhotic,
cobalt protoporphyrin and
octreotide treatment groups. The expression levels of hepatic HO-1
mRNA were measured by reverse-transcription polymerase chain reaction, while the
protein expression was determined by western blotting and immunohistochemical analysis.
Hematoxylin and
eosin, and Van Gieson's staining, along with determination of the
hydroxyproline content in the liver, were performed to determine the degree of
liver fibrosis. The serum levels of
alanine aminotransferase (ALT),
aspartate aminotransferase (AST), total
bilirubin (TBIL) and
carboxyhemoglobin (COHb) in arterial blood, and the mean arterial pressure and portal vein pressure were also measured. As compared with the
sham group, hepatic HO-1
mRNA and
protein expression levels, serum levels of ALT, AST and TBIL, COHb in arterial blood,
hydroxyproline and
collagen type I content were all significantly increased in the cirrhotic group. As compared with the cirrhotic group, the
octreotide-treated group exhibited significantly reduced hepatic HO-1 expression levels, serum levels of ALT, AST and TBIL, COHb in arterial blood and the extent of hepatic
fibrosis, whereas the
cobalt protoporphyrin group exhibited significantly increased hepatic HO-1 expression levels, as well as aggravated hepatic function and
fibrosis (P<0.05). In conclusion,
octreotide inhibited hepatic HO-1 overexpression in cirrhotic rats, reduced hepatic HO-1 expression levels to relieve liver injury and attenuated
liver fibrosis.