Molecular analysis of caspase3, smad1, bmp2 and bcl-xl genes in renal ischemia and reperfusion model in rats

Because inadequte perfusion of body part and tissue due to ischemia arterial or reduction of venous blood flood, it is defined that the body part and tissue mentioned are empty of oxygen. Reperfusion of ischemic tissue causes a crucially damage in comparison of damage happened with ischemia paradoxically in the tissue. Many mechanism play an important role in the death of cell that caused by both regeneration of cell and a new blood flood which is required to be cleaned up toxic metabolite after ischemia. In this study, levels of the genes of smad1, bmp2, bcl-XL and caspase3 have been researched for molecular changes in kidney tissues which were applied nephrectomy after the model ischemia/reperfusion (I/R) that created in kidney. For that, 30 wistar albino rats were divided equally. Group I=ischemia group (ischemia for 60 minutes+reperfusion for 48 hours) (n:10), Group II=ischemia (ischemia for 60 minutes+reperfusion for 48 hours)+calcium channel inhibitor (n:8), Group III=Ischemia (ischemia for 60 minutes+ reperfusion for 48 hours)+sodium channel inhibitor (n:8) were given pre-treatment and determined as treatment groups. According to the results of gene levels, the genes of bmp2, bcl-xL and caspase3 in treatment groups are significant statistically but smad is not significant statistically (p?0,05). In our histopathologic results, when we compared between treatment group that was given calcium channel blocker (Group II) and ischemia group in the final of the evaluation and scoring of general tissue done with hematoxylin eosin, we came to the conclusion that verapamilin which was given as calcium channel inhibitor put the death of cell down in kidney tissue.Key words: Apoptosis, bmp2, renal ischemia, smad1, verapamil