Korean J Anesthesiol.  2023 Aug;76(4):357-367. 10.4097/kja.23081.

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

• Cho JD
• Jung H
• Lee JE
• Choi EK
• Kim HA
• Ri HS
• Kim H
• Park JY
• Kwak KH
• Lim DG

• KMID: 2544555
• DOI: http://doi.org/10.4097/kja.23081

Abstract

Background
Remote ischemic postconditioning (RIPoC) is induced by several cycles of brief, reversible, mechanical blood flow occlusion, and reperfusion of the distal organs thereby protecting target organs. We investigated if RIPoC ameliorated liver injury in a lipopolysaccharide (LPS)-induced endotoxemic rats.
Methods
Protocol 1) Rats were administered LPS and samples collected at 0, 2, 6, 12, and 18 h. 2) After RIPoC at 2, 6, and 12 h (L+2R+18H, L+6R+18H, and L+12R+18H), samples were analyzed at 18 h. 3) RIPoC was 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). 4) Rats were assigned to a control group while in the RIPoC group, RIPoC was performed at 2, 6, 10, and 14 h, with samples analyzed at 18 h.
Results
Protocol 1) Liver enzyme, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), and nuclear factor-κB (NF-κB) levels increased while superoxide dismutase (SOD) levels decreased over time. 2) Liver enzyme and MDA levels were lower while SOD levels were higher in L+12R+18H and L+6R+18H groups when compared with L+2R+18H group. 3) Liver enzyme and MDA levels were lower while SOD levels were higher in L+2R+6H and L+6R+12H groups when compared with L+2R+12H and L+2R+18H groups. 4) Liver enzyme, MDA, TNF-α, and NF-κB levels were lower while SOD levels were higher in RIPoC group when compared with control group.
Conclusions
RIPoC attenuated liver injury in the LPS-induced sepsis model by modifying inflammatory and oxidative stress response for a limited period.

Keyword

Antioxidants; Ischemia reperfusion injury; Lipopolysaccharide; Malondialdehyde; Nuclear factor-κB; Sepsis; Superoxide dismutase; Tumor necrosis factor-α