Research Article Adalimumab Ameliorates Abdominal Aorta Cross Clamping Which Induced Liver Injury in Rats Erkan Cure, 1 Medine Cumhur Cure, 2 Levent Tumkaya, 3 Yildiray Kalkan, 3 Ibrahim Aydin, 4 Aynur Kirbas, 2 Arif Yilmaz, 5 Suleyman Yuce, 1 and Ahmet Fikret Yücel 4 1 Department of Internal Medicine, School of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey 2 Department of Biochemistry, School of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey 3 Department of Histology and Embryology, School of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey 4 Department of Surgery, School of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey 5 Department of Gastroenterology, School of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey Correspondence should be addressed to Erkan Cure; erkancure@yahoo.com Received 20 October 2013; Revised 9 December 2013; Accepted 15 December 2013; Published 16 January 2014 Academic Editor: Engin Erturk Copyright © 2014 Erkan Cure et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. he aim of this study was to investigate the possible protective efects of adalimumab (ADA) on cell damage in rat liver tissue during ischemia/reperfusion (I/R) injury of infrarenal abdominal aorta. hirty male Wistar-albino rats were divided into three groups: control, I/R, and I/R+ADA, each group containing 10 animals. Laparotomy without I/R injury was performed in the control group animals. Laparotomy in the I/R group was followed by two hours of infrarenal abdominal aortic cross ligation and then two hours of reperfusion. ADA (50mg/kg) was administered intraperitoneally as a single dose, to the I/R+ADA group, ive days before I/R. he tumor necrosis factor-alpha (TNF-) (pg/mg protein) and nitric oxide (NO) (mol/g protein) levels in the I/R group (430.8 ± 70.1, 8.0 ± 1.1, resp.) were signiicantly higher than those in the I/R+ADA group (338.0 ± 71.6,  = 0.006; 6.3 ± 1.2,  = 0.008) and the control group (345.5 ± 53.3,  = 0.008; 6.5 ± 1.5,  = 0.010, resp.). I/R causes severe histopathological injury to the liver tissue, but ADA leads to much less histopathological changes. ADA treatment signiicantly decreased the severity of liver I/R injury. ADA pretreatment may have protective efects on experimental liver injury. 1. Introduction Hepatic ischemia/reperfusion (I/R) injury afects the prog- nosis of patients in a vast clinical range, including trans- plantation, liver resection surgery, trauma and hemorrhagic shock, and aortic injury during abdominal surgery [1]. While aortic occlusion is carried out, the blood supply is occluded to organs such as the liver. he obstruction of the aorta and consequent reperfusion leads to distant organ injury via multiple mechanisms including neutrophilic iniltra- tion, the production of reactive oxygen species (ROS), the release of cytokines such as the tumor necrosis factor-alpha (TNF-) and elevation of nitric oxide (NO) levels [2–4]. Also, decreased arginase and carbamoyl phosphate synthetase-1 (CPS-1) enzyme activities are associated with tissue injury by elevated NO levels [5–8]. Reperfusion injury occurs ater permitting blood relow into an ischemic tissue, and the surge of oxygen to low oxygenated tissues causes an increased production of ROS [9]. he apoptosis pathway is activated as a result of mitochondrial damage due to increased ROS. Apoptosis plays a major role in liver injury induced by I/R [10]. TNF- is a pleiotropic cytokine that has biological efects ranging from cell death to inducing tissue regeneration [11– 13]. TNF- is released at the beginning of reperfusion, and its level increases during the early phases of I/R [14]. he inhibi- tion of TNF- release, or its neutralization with anti-TNF- antibodies, decreases the number of neutrophils iniltrating the liver, reducing liver I/R injury [15]. Adalimumab (ADA), which is the irst fully human monoclonal antibody targeted against TNF-, was irst administered to study patients in 1997. It has been reported that it can be safely used for Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 907915, 8 pages http://dx.doi.org/10.1155/2014/907915