Comparison of the protective effects of infliximab and splenectomy on hepatic ischemia-reperfusion injury in rats: an experimental study
- Author:
Shiback LEE
1
;
Deokhee LEE
;
Youngjun JANG
;
Dong Gun LIM
;
Kyung Hwa KWAK
;
Hoon JUNG
;
Eun Kyung CHOI
Author Information
- Publication Type:Original article
- From: Journal of Yeungnam Medical Science 2025;42(1):72-
- CountryRepublic of Korea
- Language:0
-
Abstract:
Background:Hepatic ischemia-reperfusion injury (IRI) is a complex process involving multiple mediators that initiate inflammatory responses, ultimately leading to cell necrosis and apoptosis. During hepatic IRI, various inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), and reactive oxygen species (ROS) exacerbate liver injury. Infliximab is an antibody that neutralizes TNF-α, and suppression of TNF-α activity with infliximab treatment can protect the liver from IRI. Splenectomy also alleviates hepatic IRI by decreasing neutrophil infiltration, reducing the release of ROS into the hepatic sinusoids, and suppressing TNF-α release. This study aimed to evaluate the effects of infliximab on hepatic IRI based on inflammatory responses, oxidative stress, and apoptosis, and to compare these effects with those of splenectomy.
Methods:Twenty-four rats were randomly assigned to the following four groups: (1) sham, (2) hepatic ischemia-reperfusion (IR), (3) hepatic IR with 10 mg/kg infliximab, and (4) hepatic IR with splenectomy. Each group consisted of six rats. Hepatic ischemia was induced for 30 minutes, followed by 2 hours of reperfusion injury. Infliximab was administered intraperitoneally 1 hour before surgery and splenectomy was performed immediately before hepatic ischemia.
Results:Infliximab and splenectomy downregulated the levels of liver enzymes (aspartate aminotransferase [p<0.001 for all] and alanine aminotransferase [p<0.001 for all]), a prooxidant (malondialdehyde [p=0.006 for infliximab; p<0.001 for splenectomy]), inflammatory cytokines (TNF-α and nuclear factor kappa B [p<0.001 for all]), and an apoptotic mediator (caspase-3 [p=0.005 for infliximab; p=0.004 for splenectomy]) compared with those with hepatic IR alone.
Conclusion:Infliximab treatment and splenectomy mitigated hepatic IRI. These protective effects are likely mediated via anti-inflammatory, antioxidative, and antiapoptotic pathways within the pathophysiology of hepatic IRI.
