Is adalimumab protective in ischemia-reperfusion injury in lung?

Authors

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

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 9 rats). To the control group, only laparotomy procedure was carried out. For I-R group, first infrarenal abdominal aorta was cross-clamped during 2 hr, and then reperfusion was performed for 2 hr. To I-R+Ada group, first a single dose of 50 mg/kg Ada was given intraperitoneally and 5 days later, same I-R procedure was carried out. Results:Levels of TNF-α, malondialdehyde (MDA), myeloperoxidase (MPO), endothelin-1 (ET-1) and caspase-3 enzyme activity of I-R group were higher than that of both I-R+ Ada [TNF-α (P=0.021), MDA (P=0.029), MPO (P=0.012), ET-1 (P=0.036, caspase-3 (P=0.007), respectively] and control group [TNF- α (P=0.008), MDA (P

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Journal title

volume 18  issue 11

pages  1093- 1099

publication date 2015-11-01

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