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Fatemeh Safari, Sohrab Hajizadeh, Yaghoub Fathollahi, Hossein Azizi,
Volume 10, Issue 4 (Winter 2007)
Abstract

Introduction: The relation between morphine and nitric oxide release has been shown. Due to important role of nitric oxide in regulation of skin blood flow, the aim of this study was to investigate the effect of nitric oxide synthase inhibitor (L-NAME) and nitric oxide synthesis precursor (L-arginine) on skin blood flow of intact and morphine-dependent rats. Methods: Skin blood flow of hind paw was measured using Laser Doppler Flowmetry (LDF) technique. Animals became morphine dependent by a well established protocol. Results: Subcutaneous injection of L-arginine (10 or 20 mg/kg) respectively increased skin blood flow by 39% and 64% in intact rats and by 37% and 65% in morphine-dependent rats. There was no significant difference between blood flow in intact and morphine-dependent rats. L-NAME (1 or 5 mg/kg) diminished skin blood flow of intact rats by 35% and 58.7% and skin blood flow of morphine-dependent rats by 29.1% and 60.5%, respectively. There was no significant difference between these two groups. The effect of L-arginine was abolished by pretreatment with L-NAME in morphine-dependent as well as intact groups. Conclusion: Our results suggest that changes in the level of nitric oxide, cause the same skin blood flow alterations in both morphine-dependent and intact rats. More experiments are needed to elucidate the level of nitric oxide release in skin vascular system following dependency.
Mir-Shahram Safari, Abbas Haghparast, Saeed Semnanian, Abolhassan Ahmadiani,
Volume 15, Issue 1 (Spring 2011)
Abstract

Introduction: Previous studies have shown that stimulation of lateral hypothalamus (LH) produces antinociception. Orexin-A (OXA) receptor is strongly expressed in the nucleus locus coeruleus (LC) and orexinergic fibers densely project from LH to LC. In this study, we assessed the role of LC and its OXA receptors in antinociceptive response induced by LH chemical stimulation in the rat. Methods: The cholinergic agonist carbachol (125nmol/0.5μl saline) and lidocaine (2% 0.5μl) were unilaterally microinjected into the LH with the concurrent LC inactivation. In another set of experiments, SB-334867 an OXA selective antagonist or its vehicle were unilaterally infused in LC to study its effect on LH stimulation-induced antinociception. Antinociceptive responses were obtained by the tail flick test and were presented as maximal possible effect (MPE) at 5, 10, 15, 20, 30 and 60 min after drug administrations. Results: The results showed that microinjection of carbachol into the LH significantly induced antinociception at 5 and 10 min (p<0.001). This effect was significantly blocked by microinjection of lidocaine into the LC. Additionally, intra-LC administration of SB-334867 (4.5 μg) could suppress the LH stimulation-induced antinociception by carbachol at 5 and 10 min post-injection times (p<0.001). Conclusion: Our findings showed that analgesic response induced by LH stimulation is mediated in part by the subsequent activation of LC neurons and results from the activation of orexinergic inputs into the LC that can modulate the pain processing.
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.
Shahnaz Shekarforush, Ali Noroozzadeh, Fatemeh Safari, Leila Golmanesh, Ali Khoshbaten,
Volume 15, Issue 2 (Summer 2011)
Abstract

Introduction: It has been reported that traumas such as transverse abdominal incision before myocardial ischemia result in a significantly decreased infarct size. This phenomenon is named remote preconditioning of trauma. Since small skin burn is one of most common traumas, the effect of this injury on ischemia-induced arrhythmias and infarct size was investigated in a rat model of ischemia-reperfusion injury. Methods: Twenty-four male Wistar rats were randomly assigned to 3 groups. In burn and sham groups, less than 1% of total body surface area of the dorsal skin was exposed to 100 ˚C and 37 ˚C water, respectively. In ischemic preconditioning group, rats were exposed to one cycle of ischemia (5 min) and reperfusion (10 min). Ischemiareperfusion injury was induced with occlusion and release of left coronary artery for 30 and 120 min, respectively. Infarct size was measured using triphenyl tetrazolium chloride staining and arrhythmias were assessed in accordance with Lambeth conventions. Results: Infarct size was significantly reduced in ischemic preconditioning group compared with the sham group (27 ± 2% vs. 50 ± 5% P < 0.01). Infarct size in the burn group was not significantly reduced. Irreversible ventricular fibrillation was 50% of all ventricular fibrillation in the burn group, while it was 25% in the sham group, however, this difference was not significant. Conclusion: Acute minor coetaneous burn has neither protective nor harmful for the rat myocardial ischemiareperfusion injury.
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.
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.
Mohsen Sharifi Klishadi, Farideh Zarei, Shahnaz Shekarforoush, Fereshteh Safari, Fatemeh Safari,
Volume 18, Issue 2 ( Summer 2014)
Abstract

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
Sara Sadeghzadeh, Seyed Hasan Hejazian, Mohabbat Jamhiri, Zeynab Hafizibarjin, Salman Sadeghzadeh, Fatemeh Safari,
Volume 22, Issue 1 (Winter 2018)
Abstract

Introduction: Cardiomyocytes apoptosis contributes to the development of left ventricular hypertrophy. The Bcl-2 family members are important regulators of mitochondrial pathway of apoptosis. Monoterpenoid phenol –carvacrol– possesses strong antioxidant properties. The present study aimed to evaluate the effect of carvacrol on transcription level of pro-apoptotic (Bad and Bax) and anti-apoptotic (Bcl-2 and BCL-xL) members of Bcl-2 family in hypertrophied hearts. Methods: Male Wistar rats (170-200 g) were divided into the following groups: (I) intact animals served as the control (Ctl), (II) un-treated rats subjected to aortic banding to induce left ventricular hypertrophy (H group), (III, IV, V and VI): carvacrol (C)-pretreated rats (5, 10, 25 and 50 mg/kg/day) subjected to aortic banding (H+C5, H+C10, H+C25 and H+C50 groups, respectively). Blood pressure was recorded through the carotid artery cannulation. Fibrosis was assessed by Masson’s trichrome staining. Gene expression was evaluated by real time-PCR technique. Results: In the H+C10, H+C25 and H+C50 groups mean arterial pressure (P<0.05, P<0.001 and P<0.001, respectively) and heart weight to body weight ratio (P<0.05, P<0.01 and P<0.001, respectively) were decreased significantly in comparison with H group. In the H group the Bad mRNA level was increased significantly compared to Ctl (P<0.001); while in the H+C10, H+C25 and H+C50 groups Bad mRNA level was decreased significantly (P<0.0 5, P<0.001 and P<0.001 vs. H). In H+C25 and H+C50 groups Bcl-2 and Bcl-xL mRNA were also up-regulated when compared with Ctl. Conclusion: Taken together, our results suggest that carvacrol may protect the hypertrophied heart against apoptosis by affecting transcription of Bcl-2 family members.



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