Is adalimumab protective in ischemia-reperfusion injury in lung?

Abstract

<em>Objective(s):</em> 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. <em>Materials and Methods:</em>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. <br/><em>Results</em><em>:</em>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 (<em>P</em>=0.021), MDA (<em>P</em>=0.029), MPO (<em>P</em>=0.012), ET-1 (<em>P</em>=0.036, caspase-3 (<em>P</em>=0.007), respectively] and control group [TNF- α (<em>P</em>=0.008), MDA (<em>P</em><0.001), MPO (<em>P</em>=0.001), ET-1 (<em>P</em><0.001), caspase-3 (<em>P</em><0.001), respectively]. In I-R group, severe damage was detected by hematoxylin-eosin staining. This damage was found less severe in Ada treatment group. <br/><em>Conclusion:</em>The release of cytokines and ET-1 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.