title: [Protective effects of luteolin preconditioning on rat liver under ischemia/reperfusion].
abstract: 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.
authors.affiliation: Department of Pathophysiology, Wannan Medical College, Wuhu 241002, China. guoguangw1226@sina.com
authors.forename: Guo-Guang
authors.initials: GG
authors.lastname: Wang
authors.forename: Xiao-Hua
authors.initials: XH
authors.lastname: Lu
authors.forename: Min
authors.initials: M
authors.lastname: Ding
authors.forename: Wen-Tian
authors.initials: WT
authors.lastname: Tang
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Xue
authors.initials: X
authors.lastname: Zhao
authors.forename: Cui
authors.initials: C
authors.lastname: Zhang
mesh_terms: D000818:Animals; D005260:Female; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D008099:Liver / Q000098:blood supply*; D047311:Luteolin / Q000627:therapeutic use*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D013482:Superoxide Dismutase; D047311:Luteolin