is adalimumab protective in ischemia-reperfusion injury in lung?

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<0.001), mpo (p=0.001), et-1 (p<0.001), caspase-3 (p<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. conclusion: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.