Remote Preconditioning on Rat Hepatic Ischemia–Reperfusion Injury Downregulated Bax and Cleaved Caspase-3 Expression

Abstract Objective Hepatic ischemia-reperfusion injury (IRI) is considered a major cause of hepatic damage in liver surgery. The aim of this study was to investigate the effect of the remote ischemic perconditioning method on hepatic IRI in a rat model. Methods Seventeen rats underwent hepatic IRI for 30 minutes followed by reperfusion, and were divided into 3 groups: group I, only hepatic IRI (n = 5); group II, hepatic IRI with remote perconditioning (n = 7); and group III, hepatic IRI with remote postconditioning (n = 5). Results For Bax /β-actin, mean values of the 3 groups (±standard deviation) were 1.29 ± 0.26 (group I), 0.89 ± 0.15 (group II), and 1.02 ± 0.23 (group III). The level of Bax /β-actin in group II was significantly lower than in group I ( P Caspase -3/β-actin ratio for groups I, II, and III was 0.93 ± 0.22, 0.46 ± 0.16, and 0.63 ± 0.22, respectively. The level of cleaved Caspase -3/β-actin in groups II and III were significantly lower than in group I ( P P Bcl -2/β-actin ratio for groups I, II, and III was 1.01 ± 0.09, 1.19 ± 0.39, and 1.20 ± 0.12, respectively. However, there were no significant difference between groups II and III and group I. Conclusions The remote perconditioning on rat hepatic IRI downregulated the Bax and cleaved Caspase -3 expression.