Microarray analysis of liver gene expression before and after induced hemorrhagic shock in a rat model

Cell proliferation, renewal, and apoptosis factors are related to hemorrhagic shock (HS) survival.

Hepatic gene expression before and 24 h after induced HS were compared.

Male Sprague-Dawley rats aged 8-9 wk (n = 11) were subjected to blood loss, and HS was induced in 9 rats (blood loss <0.1 mL) by left lobular hepatectomy with fixed-volume blood loss (2.5 mL/100 g) for this self-controlled study. In 3 randomly selected rats surviving >24 h post-HS, hepatic tissue samples collected pre-HS (n = 3; group A) and 24 h post-HS (n = 3; group B) were used for microarray analysis (21,793 genes) of differentially expressed genes using pathway, gene ontology, and network analyses. Real-time reverse transcriptase polymerase chain reaction confirmed Aldh1a1, Aldh1a7, amine oxidase, copper containing 3, cytochrome P450 26A1, histidine decarboxylase 1, and epoxide hydrolase 2 expression using a beta-actin reference.

Four rats survived 24 h after HS. Microarray revealed 562 upregulated and 634 downregulated genes in group A compared with group B. Gene ontology analysis revealed differentially expressed genes involved in cholesterol metabolic processes, extracellular stimuli response, sterol metabolic processes, hormonal stimuli response, steroid metabolic processes, endogenous stimulus response, oxidation and reduction reactions, organic substance response, and fatty acid metabolic processes.

HS pathogenesis involves numerous interrelated signaling pathways. Redox reaction and fatty acid metabolism pathway involvement in traumatic HS recovery, as well as other pathways, may provide novel targets for better understanding the pathology of HS and developing treatments to limit post-HS organ failure.