Fatemeh Safari1, Gholamreza Bayat2, Shahnaz Shekarforoush3, Seyedhossein Hekmatimoghaddam4, Zahra Anvari5, Mahdi Forouzandeh Moghadam6, Sohrab Hajizadeh7. 1. Yazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran Department of Physiology, Tarbiat Modares University, Tehran, Iran. 2. Department of Physiology, Tarbiat Modares University, Tehran, Iran Department of Physiology and Pharmacology, Faculty of Medical Sciences, Alborz University of Medical Sciences, Karaj, Iran. 3. Islamic Azad University, Arsanjan Branch, Fars, Iran. 4. Department of Laboratory Sciences, School of Paramedicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 5. Yazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 6. Department of Biotechnology, Tarbiat Modares University, Tehran, Iran. 7. Department of Physiology, Tarbiat Modares University, Tehran, Iran Institute for Cognitive Science Studies (ICSS), Tehran, Iran fa.cardio@gmail.com.
Abstract
BACKGROUND AND AIMS: The aim of this study was to investigate the early changes of cardiac uncoupling protein-2 (UCP2) expression following myocardial ischemia reperfusion in rats chronically treated with ramiprilat and losartan. METHODS: Male Wistar rats were assigned into seven groups (six in each): intact (control); sham-operated; nontreated rats subjected to ischemia and reperfusion (IR); ramiprilat-treated rats with (Ram+IR) and without ischemia (Ram); losartan treated with (Los+IR) and without ischemia (Los). Quantitative evaluation of UCP2 mRNA was carried out using real-time reverse transcription-polymerase chain reaction (RT-PCR). Mitochondria were isolated, and protein expression was quantified by Western blotting. RESULTS: In IR group: UCP2 protein but not mRNA level was increased in the ischemic area of the left ventricle (LV) (172% ± 26.7, p < 0.001 vs. LV of control). Following acute myocardial IR, UCP2 protein levels was increased in the ischemic area of the LV but not in RV, suggesting the local effect of ischemia on UCP2 expression. IR-induced overexpression of UCP2 was suppressed by ramiprilat and losartan. CONCLUSION: These findings suggest that losartan and ramiprilat can suppress UCP2 expression following myocardial IR, and by this mechanism may protect the myocardium against IR injury.
BACKGROUND AND AIMS: The aim of this study was to investigate the early changes of cardiac uncoupling protein-2 (UCP2) expression following myocardial ischemia reperfusion in rats chronically treated with ramiprilat and losartan. METHODS: Male Wistar rats were assigned into seven groups (six in each): intact (control); sham-operated; nontreated rats subjected to ischemia and reperfusion (IR); ramiprilat-treated rats with (Ram+IR) and without ischemia (Ram); losartan treated with (Los+IR) and without ischemia (Los). Quantitative evaluation of UCP2 mRNA was carried out using real-time reverse transcription-polymerase chain reaction (RT-PCR). Mitochondria were isolated, and protein expression was quantified by Western blotting. RESULTS: In IR group: UCP2 protein but not mRNA level was increased in the ischemic area of the left ventricle (LV) (172% ± 26.7, p < 0.001 vs. LV of control). Following acute myocardial IR, UCP2 protein levels was increased in the ischemic area of the LV but not in RV, suggesting the local effect of ischemia on UCP2 expression. IR-induced overexpression of UCP2 was suppressed by ramiprilat and losartan. CONCLUSION: These findings suggest that losartan and ramiprilat can suppress UCP2 expression following myocardial IR, and by this mechanism may protect the myocardium against IR injury.
Authors: Lukas J Motloch; Tina Gebing; Sara Reda; Astrid Schwaiger; Martin Wolny; Uta C Hoppe Journal: J Membr Biol Date: 2016-07-01 Impact factor: 1.843