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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey
MOLECULAR ANALYSIS OF SMAD-1, BMP-2, BCL-XL AND CASPASE-3 GENES IN RENAL ISCHEMIA-REPERFUSION MODEL IN RATS
Abstract number: PC024
Bulut1 Ahmed, Demir1 Tuncer, Cengiz1 Beyhan, Tutar2 Ediz, Oztuzcu3 Serdar, Yasir Bahar2 Abdulkadir, Demiryurek1 [Scedil]eniz, Dusmez1 Duygu, Nur Dagli1 [Scedil]eyda, Bagci1 Cahit
1Department of Physilogy, Gaziantep University, Gaziantep, Turkey
2Department of Pathology, Gaziantep University, Gaziantep, Turkey
3Department of Medical Biology, Gaziantep University, Gaziantep, Turkey
Objective:
In this study, we aimed to investigate the effects of Smad-1 (TGF super family) and BMP-2 genes in renal Ischemia-Reperfusion (I/R) model in rats. Furthermore, we aimed to investigate the gene levels of Caspase-3 (affected by apoptotic) and Bcl-xL (affected by antiapoptotic) genes to find out the possible apoptotic effects of Smad1 and BMP2 in the kidney.
Methods:
Forty female rats were allocated into sham, ischemia, ischemia+Ca channel blocker and ischemia+Na channel blocker groups. The ischemia group did not receive any treatment. Other groups received Ca channel blocker or Na+ channel blocker before 30 minutes of anesthesia. Then, the abdomen was opened with a midline incision and bilateral renal arters were clamped for 60 minutes. After 48 hour reperfusion, blood samples and kidney tissues were collected. Tissue samples were examined by histopathological and RT-PCR methods for the expression levels of Smad-1, Bmp-2, Bcl-xL and Caspase-3.
Results:
There was a significant histopathologial difference between the calcium channel blocker group and other groups. On the other hand, Bcl-xL gene was significantly different from Smad-1, Bmp-2 and Caspase-3 genes according to the moleculer analyses.
Conclusions:
Calcium channel blockers may ameliorate the renal ischemia-reperfusion injury. These agents may be beneficial after controlled clinical studies.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC024