Aysel Kurt - RecepTayyip Erdogan University, School of Medicine, Department of Thoracic Surgery, Rize, Turkey
Levent Tumkaya - RecepTayyip Erdogan University, School of Medicine, Department of Histology and Embryology, Rize, Turkey
Yildiray Kalkan - RecepTayyip Erdogan University, School of Medicine, Department of Histology and Embryology, Rize, Turkey
Hasan Turut - RecepTayyip Erdogan University, School of Medicine, Department of Thoracic Surgery, Rize, Turkey
Medine Cumhur Cure - RecepTayyip Erdogan University, School of Medicine, Department of Biochemistry, Rize, Turkey
Erkan Cure - RecepTayyip Erdogan University, School of Medicine, Department of Internal Medicine, Rize , Turkey
Ibrahim Sehitoglu - RecepTayyip Erdogan University, School of Medicine, Department of Pathology, Rize, Turkey
Hacer Bilgin - RecepTayyip Erdogan University, School of Medicine, Department of Biochemistry, Rize, Turkey
Mustafa Usta - RecepTayyip Erdogan University, School of Medicine, Department of Internal Medicine, Rize , Turkey

Objective(s): Increasing cytokines and reactive oxygen species (ROS) during ischemia reperfusion (I-R) leads to the lung damage. Adalimumab (Ada) is a potent tumor necrosis factor-alpha (TNF-α) inhibitor agent. We aimed to evaluate whether Ada would prevent the lung tissue from damage development over the I-R process. Materials and Methods:Twenty seven Wistar albino male rats were divided into three groups (each group had ۹ rats). To the control group, only laparotomy procedure was carried out. For I-R group, first infrarenal abdominal aorta was cross-clamped during ۲ hr, and then reperfusion was performed for ۲ hr. To I-R+Ada group, first a single dose of ۵۰ mg/kg Ada was given intraperitoneally and ۵ days later, same I-R procedure was carried out. Results:Levels of TNF-α, malondialdehyde (MDA), myeloperoxidase (MPO), endothelin-۱ (ET-۱) and caspase-۳ enzyme activity of I-R group were higher than that of both I-R+ Ada [TNF-α (P=۰.۰۲۱), MDA (P=۰.۰۲۹), MPO (P=۰.۰۱۲), ET-۱ (P=۰.۰۳۶, caspase-۳ (P=۰.۰۰۷), respectively] and control group [TNF- α (P=۰.۰۰۸), MDA (P<۰.۰۰۱), MPO (P=۰.۰۰۱), ET-۱ (P<۰.۰۰۱), caspase-۳ (P<۰.۰۰۱), respectively]. In I-R group, severe damage was detected by hematoxylin-eosin staining. This damage was found less severe in Ada treatment group. Conclusion:The release of cytokines and ET-۱ in a large proportion after I-R injury, and generating of ROS in excessive quantity could cause severe damage in the lung tissue. Ada could be considered as a protective agent for lung tissue during I-R process.

Adalimumab, Endothelin-۱, Ischemia reperfusion, Lung injury, Tumor necrosis factor-alpha