The aim of the study is to explore the effects of
luteolin preconditioning on hepatic
ischemia/reperfusion injury in rats and its mechanism, and investigate the effects of the change of
heme oxygenase-1 (HO-1) activity on hepatic
ischemia/reperfusion injury. Sprague-Dawley rats were divided into 5 groups randomly: control, model,
luteolin,
luteolin +
zinc protoporphyrin (ZnPP, an inhibitor of HO-1) and
hemin groups (n = 8 for each group). The rats in control, model and
hemin groups received a standard chow daily. The rats in
luteolin and
luteolin + ZnPP groups received a chow supplemented with
luteolin (200 mg/kg) daily. After 4 weeks, ZnPP (25 μmol/kg) and
hemin (20 μmol/kg) were injected hypodermically 6 h before
ischemia/reperfusion in
luteolin + ZnPP and
hemin groups, respectively. Portal vein and hepatic artery supplying the middle and left hepatic lobe were clamped with an atraumatic vascular
clip for induction of partial hepatic
ischemia in all rats except control group. After the 60 min of hepatic
ischemia, a 60-minute reperfusion period was initiated by removal of the arterial
clip. The levels of
aspartate aminotransferase (AST) and
alanine aminotransferase (ALT) were detected in serum, and the activity of
superoxide dismutase (SOD) and the content of
malondialdehyde (MDA) in serum and liver were measured with assay kit. The expression of HO-1
protein and activity of HO-1 were examined in liver. The results showed that the
luteolin and
hemin pretreatment led to significant decreased levels of AST and ALT in serum, increased activity of SOD and decreased content of MDA in serum and liver compared with model group (P < 0.01). In addition, the expression of HO-1
protein and activity of HO-1 were elevated in
luteolin and
hemin groups (P < 0.01). ZnPP markedly increased the levels of AST and ALT in serum, and decreased the activities of SOD and HO-1, elevated MDA content in liver when compared with those in
luteolin group (P < 0.01). Cytoplasmic vacuolation and swelling of hepatocytes were revealed in the model group after
ischemia/reperfusion. Treatments with
luteolin and
hemin markedly relieved the liver structural changes. These results suggest that HO-1 protects rat liver from
ischemia/reperfusion injury, and
luteolin reduces the content of MDA and increases the activity of SOD and the expression of HO-1, which indicate that
luteolin can elevate the antioxidation in rat liver, and thus protects rat liver from
ischemia/reperfusion injury.