Experimental Studies On The Protective Effect Of Thyroid Hormone Against Hepatic Ischemia-reperfusion Injury In Rat

Objective: To investigate the protective effect of thyroid hormone against hepatic ischemia reperfusion injury in rat and its possible mechanism.Methods: The model of 70% hepatic ischemia-reperfusion was established in rat. Sixty-four healthy male SD rats were randomly divided into 4 groups, S: sham operation group;IR: ischemia-reperfusion group;IPC: ischemic preconditioning group;T3: thyroid hormone treatment group. Except that S group, the blood supply of the middle and left liver lobe were blocked by a microvascular clip for 1 h in other three groups, about 70% of the liver underwent ischemia. In T3 group, T3 (0.1mg/kg) was intraperitoneal injected at 48 h before ischemia; in IPC group, 10 min of ischemic preconditioning and 10 min of reperfusion before ischemia. After 6h,24h of reperfusion, aspartate aminotransferase(AST),alanine aminotransferase (ALT) levels were measured in the serum;The superoxide dismutase (SOD) activity,levels of malondialdehyde(MDA) and glutathione (GSH) in the hepatic tissue were detected. And tumor necrosis factor alpha (TNF-α) levels were detected by ELISA. Histologic changes were observed in HE staining, and the expression of NF-κB in liver cells was evaluated by immunohistochemistry.Results: After ischemia-reperfusion, compared to S group, IR group showed high levels of ALT,AST,MDA,TNF-αand NF-κB expression and obviously injury of liver tissue, but the activity of SOD and GSH was decreased. After treatment of thyroid hormone and ischemic preconditioning, The levels of ALT,AST,MDA,TNF-αand NF-κB expression and the injury of liver tissue were declined, and the activity of SOD and GSH was increased. (P < 0.01).but there are no obvious difference between IPC group and T3 group (P >0.05).Conclusion: Thyroid hormone, as well as ischemic preconditioning, has a protection against hepatic ischemia-reperfusion injury in rats. The mechanism of protection associated with its scavenging of radical, inhibiting of lipid peroxidation, decreasing TNF-αlevel and suppressing of NF-κB activation.