@article { author = {Şimşek, Hasan and Demiryürek, Şeniz and Demir, Tuncer and Didem Atabay, Hüsne and Çeribasi, Ali Osman and Bayraktar, Recep and Sinan Kaplan, Davut and Öztuzcu, Serdar and Cengiz, Beyhan}, title = {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}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {19}, number = {2}, pages = {209-214}, year = {2016}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2016.6547}, abstract = {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 Smad1, Bmp-2, Bcl-XL, b-FGF, Caspase-3, TGF-β1, PDGFR-α genes for molecular changes in lung tissues, after I/R is formed, in this study. For this, we included 40 Wistar albino 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. Results: We have found a significant increase in expression of Bcl-XL (P=0.046) and Caspase-3 (P=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 b-FGF (P=0.087), Bmp-2 (P=0.457), TGF-β1 (P=0.201) and PDGFR-α (P=0.116) were not significant compared to control group. We did not see any mRNA expression of Smad1 gene in all groups include control. Conclusion: These findings suggest that I/R injury may trigger apoptotic mechanism in lung.}, keywords = {Apoptosis,Growth factors,Ischemia/Reperfusion,Lung}, url = {https://ijbms.mums.ac.ir/article_6547.html}, eprint = {https://ijbms.mums.ac.ir/article_6547_77d673394b582525b7ead558e2775b86.pdf} }