Effects of remote ischemic postconditioning on hepatic injury in lipopolysaccharide-induced endotoxemic rats.

Abstract

Remote ischemic postconditioning (RIPoC) is that several cycles of brief, reversible, mechanical blood flow occlusion and reperfusion of distal organ make protection to target organ. We investigate whether RIPoC ameliorates liver injury in lipopolysaccharide (LPS)-induced sepsis model. Protocol 1) Rats were administered LPS solution and samples were collected at 0, 2, 6, 12, and 18 h after that. Protocol 2) After RIPoC at 2, 6, and 12 h (L+2R+18H, L+6R+18H, L+12R+18H), samples were analyzed at 18 h. Protocol 3) RIPoC performed at 2 h, analysis samples at 6, 12, 18 h (L+2R+6H, L+2R+12H, L+2R+18H), and RIPoC at 6 h, analysis at 12 h (L+6R+12H). Protocol 4) Rats were divided control group, which were injected with only ketamine and RIPoC group, which RIPoC was performed at 2, 6, 10, and 14 h, samples were analyzed at 18 h. In protocol 1, liver enzymes, MDA, TNF-α and NF-kB increased, and SOD decreased over time. In protocol 2, liver enzyme and MDA level were lower and SOD level was higher in L+12R+18H and L+6R+18H groups, compared with L+2R+18H group. In protocol 3, liver enzyme and MDA level were lower and SOD level was higher in L+2R+6H and L+6R+12H groups, compared with L+2R+12H and L+2R+18H groups. In protocol 4, liver enzyme, MDA, TNF-α, and NF-kB levels were lower and SOD level was higher in RIPoC group, compared with control group. RIPoC attenuated liver injury in LPS-induced sepsis model by modifying inflammatory responses and oxidative stress response for a limited period.