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Showing 6 results for Bayat

Fatemeh Safari, Sohrab Hajizadeh, Shahnaz Shekarforush, Mehdi Forouzandeh, Mohsen Foadoddini, Gholamreza Bayat, Bita Houshmand, Ali Khoshbaten,
Volume 15, Issue 1 (Spring 2011)
Abstract

Introduction: Inhibition of renin angiotensin system represents an important approach in the management of cardiovascular diseases. The aim of this study was to explore the effects of pretreatment with non-hypotensive dose of angiotensin converting enzyme (ACE) inhibitor, ramiprilat and angiotensin type 1 (AT1) receptor blocker, losartan on myocardial infarct size and arrhythmias in a rat model of ischemia-reperfusion injury. Methods: Seventy male Wistar rats were divided into five groups. One group received saline as control. Other groups were given 10 mg/kg/day of losartan for one (L-1W) or ten weeks (L-10W) as well as 50 μg/kg/day of ramiprilat for one (R-1W) or ten weeks (R-10W) using a feeding needle. The rats were subjected to 30 minutes occlusion and 120 minutes reperfusion of the left coronary artery. Infarct size was determined using triphenyl tetrazolium chloride staining. Ischemia-induced ventricular arrhythmias were analyzed in accordance with the Lambeth conventions. Results: Myocardial infarct size and the number of ventricular beats were significantly reduced in R-1W group, but the reduction was not significant in L-1W. After increasing the duration of pretreatment to 10 weeks in L-10W group, the infarct size, the number of ventricular beats and the episodes of ventricular tachycardia were significantly decreased. However in R-10W group the reduction of ventricular arrhythmias was not significant Conclusion: Based on the above mentioned results it could be concluded that losartan and ramiprilat, at a nonhypotensive dose, can reduce the induction of arrhythmias and infarct size following myocardial ischemia reperfusion. These drugs appear to act in a time-dependent manner. Therefore, we expected an increased cardiac effect by long-term administration of losartan. However prolonged treatment with ramiprilat reduced its protective effect.
Masoomeh Mazandarani, Fatemeh Hoseini, Akhtar Seifi, Hooman Bayat, Mona Pourabouk, Fakhri Badaghabadi, Maryam Rajaei, Hamidreza Moheimani, Vahid Khori,
Volume 15, Issue 3 (Fall 2011)
Abstract

Introduction: Considering the long traditional history of anti-inflammatory and anti-spasmodic effects of Matricria spices on the gastrointestinal system, the present study aimed to investigate the role of calcium channels and Histamine receptors in the inhibitory effects of hydroalcoholic dry extract of German chamomile (Matricaria recutita L.) on the isolated rabbit jejunum. Methods: All experiments were done on the isolated jejunum of New Zealand rabbits (1.8-2.5 kg). Dry extract of aerial parts of M. recutita was obtained by the maceration technique. The study was performed on two groups (n=6 in each group). In the first group, the effects of cumulative concentrations of M. recutita (3×10-3-1×10-2 mg/ml) on normal and K+-induced contractions (50 mM) of isolated jejunum were studied. In the second group, the inhibitory role of M. recutita ( 3 – 13×10-3 mg/ml) was evaluated in the presence and absence of histamine and cetrizine. In the presence and absence of 10 μM certizine, a histamine H1-antagonist, a concentration-dependent inhibitory effect of M. recutita extract in the range of 3-13×10-3 mg/ml was recorded the rabbit jejunum. Results: Results showed that EC50 of M. recutita in the absence and presence of K+ was 6.3×10-3 and 6.5×10- 3mg/ml, respectively. IC50 values for two concentrations of M. recutita (8×10-3 , 1×10-2 ) to abrogated contractive phase of Histamine was 9.55 × 10-6 and 1.57 × 10-6 μM. Cetrizine (10 μM) abolished inhibitory effects of M. recutita (IC50=3.6×10-3), (p< 0.001). Conclusion: Dry extract of matricaria recutita had inhibitory effects on the contractions of isolated rabbit jejunum. Calcium channels and histamine were involved in these antispasmodic effects.
Gholamreza Bayat, Sohrab Hajizadeh, Mohammad Javan, Mahdi Forouzandeh Moghaddam, Fatemeh Safari, Hossein Azizi, Roham Mazloom,
Volume 15, Issue 3 (Fall 2011)
Abstract

Introduction: The effect of regular exercise in decreasing the incidence of heart diseases is well known. The abuse of anabolic androgenic steroids (AAS) has been associated with cardiovascular disorders. Uncoupling proteins (UCPs) transport protons across the inner mitochondrial membrane thereby proton gradient can be diminished by the action of UCPs. This process will result in the uncoupling of mitochondrial respiration from ATP production. The goal of this study was to investigate whether UCP2 and UCP3 are involved in the mechanisms of AAS-induced cardiac damage in the rat heart. Methods: In the current study, adult male Wistar rats were divided into five groups (n=8): Control, vehicle, nandrolone, exercise, exercise- nandrolone. Rats in the exercise groups were submitted to a progressive running program on a treadmill, 5 days a week for 10 weeks. Rats in the nandrolone and exercise- nandrolone groups received a weekly intramuscular injection of nandrolone decanoate (10 mg/kg), while those in the vehicle group received Arachiz oil as vehicle. Relative mRNA expression of UCP2 and UCP3 were determined with real-time RT- PCR. Results: The data showed that chronic administration of nandrolone significantly up-regulated UCP2 and UCP3 mRNA in rat heart and endurance training induced a decrease in the expression of UCP2 and UCP3 mRNA with or without presence of nandrolone. Conclusion: It may be concluded that chronic nandrolone treatment causes an increase in the expression of UCP2 and UCP3 mRNA. Thus, it might decrease energy metabolism efficiency by impairment of ATP production. Physical activity may decrease the adverse effects of nandrolone by down-regulation of the UCP2 and UCP3 mRNA expression.
Firoozeh Alavian, Sohrab Hajizadeh, Mohammad Reza Bigdeli, Gholam Reza Bayat, Mohammad Javan,
Volume 16, Issue 1 (Spring 2012)
Abstract

Introduction: ischemic preconditioning is one of the most important mechanisms, responsible for the increased brain resistance after stroke. One of the most important candidates to ischemia preconditioning is intermittent normobaric hyperoxia. In this study, the effect of intermittent normobaric hyperoxia on the expression of UCP2 was investigated in a stroke model. Methods: Rats were divided into 4 groups (normoxia – sham, hyperoxia – sham, normoxia – stroke and hyperoxia – stroke). Hyperoxia groups were exposed to 95% inspired O2, for 4 h/day and 6 consecutive days. Oxygen level in the control groups was %21 (normoxia). After 24 h, stroke groups were subjected to 60 min of right middle cerebral artery occlusion. After 24 h reperfusion neurological deficit scores were assessed. The brain UCP2 levels were analyzed by western blot. Results: The results of this study showed that following brain ischemia-reperfusion, UCP2 levels significantly increased in the stroke groups compared with the sham group while there was no significant difference in hyperoxia groups compared with normoxia. Also hyperoxia decreased neurological deficit scores. Conclusion: Following ischemia, oxidative stress caused by increase of ROS, leads to increased UCP2 levels in stroke groups. In this study, the neuroprotective effect of hyperoxia is independent of UCP2 expression.
Fatemeh Safari, Sohrab Hajiadeh, Seyed Hosein Moshtaghion, Mehdi Forouzandeh Moghadam, Shahnaz Shekarforoush, Gholamreza Bayat, Roham Mazlum, Leila Sattarian,
Volume 16, Issue 1 (Spring 2012)
Abstract

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)
Abstract

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.

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