Hadi Yousefi - Tuberculosis & Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Naser Ahmadiasl - Tuberculosis & Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Alireza Alihemmati - Department of Anatomy and Histology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
Parisa Habibi - Tuberculosis & Lung Research Center, Tabriz University of Medical Sciences, Tabriz, Iran

Objective(s):Acute kidney injury (AKI), a syndrome characterized by decreased glomerular filtration, occurs in every ۱ of ۵ hospitalized patients.  Renal ischemia-reperfusion, one of the main causes of AKI, is of particular importance in the setting of kidney transplantation. Materials and Methods: Sixty male rats were divided into four groups including control, nephrectomy, sham surgery and renal ischemia-reperfusion (IRI) group. The rats were anesthetized with intraperitonealketamin and xylazin. For making IRI group, right nephrectomywas performed, and after a week, the left kidney pedicle was occluded for ۴۵ min for making ischemia that followed by ۲۴ hr reperfusion. At the end of reperfusion phase, the lung tissues were isolated to be used in immunohistochemical and histological assays. Immunohistochemical assay was used to evaluate Bcl-۲ and TNF-α, and hematoxylin-eosin staining assay was used to histopathology. Results: lung tissues injury after renal ischemia-reperfusion was revealed by immunohistochemistry analysis to increase TNF-α level and decrease Bcl-۲ (an anti-apoptotic protein) level.  Lung injury and necrosis was discovered by hematoxylin-eosin staining to be more evident in IRI group than sham and control groups. Conclusion: The results demonstrated that increase in TNF-α and decrease in Bcl-۲ levels in lungs induces the pulmonary inflammatory damage in renal IRI model.

Bcl-۲, Inflammatory response, Lunginjury, Renal ischemia-reperfusion, TNF-α