Abstract

Fluid resuscitation after hemorrhagic shock is a model of systemic ischemia/reperfusion injury (SI/RI), and the liver is one of the main target organs. Ischemic preconditioning (IPC) can reduce hepatic ischemia-reperfusion injury (I/RI) via autophagy. However, whether remote ischemic preconditioning (RIPC) can alleviate the liver injury that is secondary to hemorrhagic shock and the role of autophagy in this process remain unclear. Thus, we constructed a hemorrhagic shock model in rats with or without RIPC to monitor mean arterial pressure (MAP) and investigate liver secondary injury levels via serum aminotransferase, ultrasound, HE staining and TUNEL fluorescence staining. We also detected levels of serum inflammatory factors including tumor necrosis factor-alpha (TNF-α) and interleukin 1β (IL-1β) by enzyme-linked immunosorbent assay (ELLSA), observed autophagosomes by Transmission electron microscopy (TEM), and analyzed LC3, Beclin-1, p62 protein expression levels by immunohistochemical (IHC) and western blot (WB). We found that RIPC increased blood pressure adaptability, decreased lactate (Lac) and aminotransferase levels, and delayed the decrease in liver density. Levels of inflammatory factors TNF-α, IL-1β and apoptosis were attenuated, autophagosomes was increased in the RIPC group compared with controls. IHC and WB both revealed increased LC3 and Beclin-1 but decreased p62 protein expression levels in the RIPC group. Together, our data suggest that RIPC-activated autophagy could play a protective role against secondary liver injury following hemorrhagic shock.