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

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 post conditioning (n = 5). Results. For Bax/beta-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/beta-actin in group II was significantly lower than in group I (P < .01). The cleaved Caspase-3/beta-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/beta-actin in groups II and III were significantly lower than in group I (P < .01 and P < .05, respectively). The Bcl-2 beta-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.