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.
Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.
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Background Pregabalin has been studied as a single or multimodal analgesic drug for postoperative pain management in different types of surgeries. We evaluated the analgesic effect of 150 mg of pregabalin in resolving post-gastrectomy pain.
Methods Forty-four patients were randomized into two groups: a pregabalin group that received oral pregabalin (150 mg) 2 h before anesthetic induction, and a control group that received placebo tablets at the same time. Data on postoperative pain intensity (visual analog scale [VAS], at 30 min, 2 h, 4 h, and 24 h), consumption of fentanyl in patient-controlled analgesia (PCA), and the proportion of patients requiring rescue analgesics at different time intervals (0-2 h, 2-4 h, and 4-24 h) were collected during the 24 h postoperative period.
Results The VAS scores did not show significant differences at any time point and consumption of fentanyl in PCA and the proportion of patients requiring rescue analgesics did not differ between the two groups. The groups did not differ in the occurrence of dizziness, sedation, and dry mouth.
Conclusion A preoperative 150 mg dose of pregabalin exerts no effect on acute pain after gastrectomy.
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