Hasan Şimşek - Dumlupınar University, Department of Physiology, Faculty of Medicine, Kütahya, Turkey
Şeniz Demiryürek - Gaziantep University, Department of Physiology, Faculty of Medicine, Gaziantep, Turkey
Tuncer Demir - Gaziantep University, Department of Physiology, Faculty of Medicine, Gaziantep, Turkey
Hüsne Didem Atabay - Gaziantep University, Department of Physiology, Faculty of Medicine, Gaziantep, Turkey
Ali Osman Çeribasi - Fırat University, Department of Pathology, Faculty of Veterinary Science, Elazığ, Turkey
Recep Bayraktar - Gaziantep University, Department of Medical Biology, Faculty of Medicine, Gaziantep, Turkey
Davut Sinan Kaplan - Gaziantep University, Department of Physiology, Faculty of Medicine, Gaziantep, Turkey
Serdar Öztuzcu - Gaziantep University, Department of Medical Biology, Faculty of Medicine, Gaziantep, Turkey
Beyhan Cengiz - Gazi University, Department of Medical Genetic, Faculty of Medicine, Ankara, Turkey

Objective(s):Ischemia is described as organs and tissues are destitute of oxygen due to decreased arterial or venous blood flow. Many mechanisms play role in cell death happened as a consequence of a new blood flow is needed for both cell regeneration and to clean toxic metabolites during ischemia and later. Lung damage induced by ischemia/reperfusion (I/R) is a frequent problem in lung transplantation. Apoptosis (programmed cell death) is known as cell suicide, and plays a key role in embryonic developmental and in maintain adult tissue’s life. Materials and Methods:It is investigated expressions of Smad۱, Bmp-۲, Bcl-XL, b-FGF, Caspase-۳, TGF-β۱, PDGFR-α genes for molecular changes in lung tissues, after I/R is formed, in this study. For this, we included ۴۰ Wistar albino rats to this study and divided ۴ groups (n=۱۰). The Groups were determined as Control (C), Group ۱= ۱ hr ischemia (I), Group ۲= ۱ hr ischemia+۲ hr reperfusion (I+۲R), Group ۳= ۱ hr ischemia+۴ hr reperfusion (I+۴R). Besides, molecular analysis and histopathologic examinations of tissues were performed, and the results were evaluated by normalization and statistics analysis. Results: We have found a significant increase in expression of Bcl-XL (P=۰.۰۴۶) and Caspase-۳ (P=۰.۰۲۶) genes of group ۱, and it was not monitored any significant difference in Group ۲ and Group ۳. In all groups, the changes in b-FGF (P=۰.۰۸۷), Bmp-۲ (P=۰.۴۵۷), TGF-β۱ (P=۰.۲۰۱) and PDGFR-α (P=۰.۱۱۶) were not significant compared to control group. We did not see any mRNA expression of Smad۱ gene in all groups include control. Conclusion: These findings suggest that I/R injury may trigger apoptotic mechanism in lung.

Apoptosis, Growth factors, Ischemia/Reperfusion, Lung