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Showing 3 results for Shekarforoush

Fatemeh Safari, Sohrab Hajiadeh, Seyed Hosein Moshtaghion, Mehdi Forouzandeh Moghadam, Shahnaz Shekarforoush, Gholamreza Bayat, Roham Mazlum, Leila Sattarian,
Volume 16, Issue 1 (Spring 2012)

Introduction: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (Nox2) is one of the predominant sources of ROS production during myocardial ischemia-reperfusion and can be induced by angiotensin II. The evidence suggests that pharmacological blockers of renin-angiotensin system can exert direct tissue effects independent of their ability to regulate blood pressure. The mechanism(s) responsible for such direct effects are not well understood. The aim of this study was to investigate the early changes of cardiac NOX2 gene transcription after myocardial ischemiareperfusion in rats treated with losartan, an angiotensin type 1 (AT1) receptor blocker. Methods: Wistar rats were divided into five groups: Control, sham operated, ischemia-reperfusion (group IR), losartan without ischemia and losartan with ischemia-reperfusion. The animals underwent 30 min of left anterior descending artery occlusion and subsequent reperfusion for 180 min. The mRNA expression was determined by real time-PCR in ischemic area of the left ventricle (LV) and non ischemic area of right ventricle (RV). Results: Compared to control hearts, exposure to myocardial ischemia-reperfusion produced a significant increase in NOX2 mRNA level in ischemic area of LV (P<0.001) but not in non ischemic area of right ventricle. Although in losartan group, NOX2 mRNA levels neither in LV nor RV were significantly altered, while in losartan and ischemiareperfusion group NOX2 mRNA upregulation in ischemic area was significantly suppressed (P<0.01). Conclusion: Based on the obtained results, it could be concluded that following acute myocardial ischemia– reperfusion, NOX2 mRNA levels were increased in ischemic area of left ventricle but not in non ischemic area of right ventricle, suggesting the local effect of ischemia on the gene expression. Furthermore, inhibition of NOX2 transcription in ischemic area may be a mechanism of the anti ischemia effects of losartan.
Fatemeh Safari, Gholamreza Bayat, Shahnaz Shekarforoush, Asefeh Fekri, Seyyed Hosein Moshtaghioun, Mahdi Foruzande Moghadam, Sohrab Hajizadeh,
Volume 17, Issue 2 (Summer 2013)

Introduction: Reactive oxygen species (ROS) have been suggested to play an important role in the myocardial damage induced by ischemia – reperfusion. One element believed to be activated by ROS and to contribute to the reduction of ROS production, is the uncoupling protein-2 (UCP2). The objective of this investigation was to explore the effect of myocardial ischemia reperfusion on cardiac UCP2 mRNA and protein levels. Methods: Male Wistar rats (250-300gr) were subjected to 30 min occlusion and 2 hours reperfusion of left coronary artery. The expression of UCP2 mRNA and protein in the ischemic area of left ventricle and non ischemic area from right ventricle were analyzed. The mRNA and protein expression were determined by RT-PCR and western blotting, respectively. Results: Compared to control hearts, exposure to myocardial ischemia reperfusion caused a significant increase in UCP2 protein in the ischemic area of the left ventricle (116%±18, P<0.001), however UCP2 mRNA expression did not change significantly. Furthermore, in the non ischemic area of the right ventricle, neither protein nor mRNA levels were affected by myocardial ischemia reperfusion. Conclusion: We conclude that following acute myocardial ischemia reperfusion, UCP2 protein level is increased in the ischemic area of the left ventricle but not in the non ischemic area of the right ventricle, suggesting the local effect of ischemia on UCP2 protein expression. Furthermore, the discordance between mRNA and protein expression of UCP2 suggests that post transcriptional regulation of mRNA influences protein induction.
Mohsen Sharifi Klishadi, Farideh Zarei, Shahnaz Shekarforoush, Fereshteh Safari, Fatemeh Safari,
Volume 18, Issue 2 ( Summer 2014)

Introduction: Studies support the idea that low levels of vitamin D are associated with a higher risk of heart disease. Losartan has also been prescribed as a drug commonly used for treating hypertension. The aim of the current study was to investigate the effects of 1,25-dihydroxyvitamin D in combination with a non-hypotensive dose of losartan on myocardial infarct size, reperfusion-induced arrhythmia and cardiac expression of survival factors in the ischemicreperfused rat heart. Methods: Male rats were randomly divided into untreated ischemia-reperfused rats (IR group) and groups pretreated with losartan (Los+IR) or vitamin D3 (VitD+IR) or both of them (Los+VitD+IR). Animals were subjected to 30 min of left coronary artery occlusion followed by 120 min of reperfusion. Infarct size measurement was performed using tetrazolium chloride. Incidence of arrhythmia was analysed according to Lambeth convention. Gene expression was evaluated by real time RT-PCR technique. Results: In VitD+IR and Los+IR groups the infarct size did not differ significantly. In Los+VitD+IR group, the infarct size was decreased by 21.4±7.3% (P<0.001 vs. IR, P<0.05 vs. VitD+IR, P<0.01 vs. Los+IR). The number of ventricular ectopic beats was 201±32 beats in Los+VitD+IR group (P<0.001 vs. IR, P<0.01 vs. VitD+IR, P<0.05 vs Los+IR ). The increase of thioredoxin-1 and catalase transcription levels was not significant in Los+IR and VitD+IR groups, however, in Los+VitD+IR group the mRNA levels of these survival factors were markedly increased (P<0.001 vs IR). Conclusion: Co-administration of a non-hypotensive dose of losartan and vitamin D3 protects the heart against ischemia-reperfusion injury accompanied by an increase in transcription of prosurvival factors

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