Assessment of expressions of Bcl-XL, b-FGF, Bmp-2, Caspase-3, PDGFR-α, Smad1 and TGF-β1 genes in a rat model of lung ischemia/reperfusion

Abstract

<strong><em>Objective(s):</em></strong>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. <strong><em>Materials and Methods:</em></strong>It is investigated expressions of <em>Smad1, Bmp-2, Bcl-XL, b-FGF, Caspase-3, TGF-β1, PDGFR-α</em> genes for molecular changes in lung tissues, after I/R is formed, in this study. For this, we included 40 <em>Wistar albino</em> rats to this study and divided 4 groups (n=10). The Groups were determined as Control (C), Group 1= 1 hr ischemia (I), Group 2= 1 hr ischemia+2 hr reperfusion (I+2R), Group 3= 1 hr ischemia+4 hr reperfusion (I+4R). Besides, molecular analysis and histopathologic examinations of tissues were performed, and the results were evaluated by normalization and statistics analysis. <strong><em>Results:</em></strong> We have found a significant increase in expression of <em>Bcl-XL </em>(<em>P</em>=0.046) and <em>Caspase-3 </em>(<em>P</em>=0.026) genes of group 1, and it was not monitored any significant difference in Group 2 and Group 3. In all groups, the changes in <em>b-FGF </em>(<em>P</em>=0.087), <em>Bmp-2 </em>(<em>P</em>=0.457), <em>TGF-β1 </em>(<em>P</em>=0.201) and <em>PDGFR-α </em>(<em>P</em>=0.116) were not significant compared to control group. We did not see any mRNA expression of <em>Smad1</em> gene in all groups include control. <strong><em>Conclusion:</em></strong> These findings suggest that I/R injury may trigger apoptotic mechanism in lung.