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Showing 22 results for Hajizadeh

Mohammad Rostampour, Yaghoub Fathollahi, Saeed Semnanian, Sohrab Hajizadeh, Javad Mirnajafi-Zadeh,
Volume 4, Issue 2 (Fall and Winter 2000)
Abstract

The effect of cysteamine, a somatostatin depletor, on synaptic plasticity induced by tetanic and paired-pulse stimulation was investigated in rat hippocampal CA1. For this purpose, hippocampal slices from saline (1 ml/kg, s.c.) and cysteamine (200 fig/kg, s.c.)-treated and intact rats were used. Population spikes were recorded following Schaffer collateral stimulation. To induce LTP, primed burst tetanic stimulation was used. Paired-pulse stimulation at IPIs of 10, 20, 60, 120, 240, 360, and 480 ms were used and then EPI and PPI of CA1 were calculated. The results showed that the amplitude of population spike (PSA) increased 5, 15, 30, and 60 min after tetanic stimulation and 60 min after primed bursts, PSA increased at all stimulus intensities for all groups. In cysteamine-treated group, the magnitude of LTP was decreased as compared to intact and saline-treated groups. In the latter group, the magnitude of LTP Increased as compared to Intact and cysteamme- treated group. At IPI of 10 ms, mean value of EPI was greater than 1 for intact group and less than 1 for saline- and cysteamine-treated groups. In cysteamine-treated group, the mean value of EPI was significantly less than intact group. At IPIs from 20 to 480 ms, mean value of EPI was greater than or equal to I for all of the groups and no significant difference was observed among them. At IPI of 10 ms, mean value of PPI was greater than I in intact group and less than I in saline- and cysteamine-treated groups. In these groups, mean value of PPI was significantly less than intact group. At IPI of 20 ms, mean value of PPI was greater than I in intact and saline-treated group and less than I in cysteamine-treated group. In the latter group, the mean value of PPI was significantly less than saline-treated and intact groups. At IPIs of 60-680 ms, mean value of PPI was greater than I in all of the groups with no significant difference among them. It is concluded that cysteamine can alter susceptibility of hippocampal CA1 for synaptic plasticity induced by tetanic and paired-pulse paradigms.
Mohamamd Badavi, Ali Khoshbaten, Sohrab Hajizadeh, Farzaneh Nazari,
Volume 4, Issue 2 (Fall and Winter 2000)
Abstract

The effect of chronic inflammation induced by complete Freund's adjuvant (CFA) on anterior blood vessels of knee joint and its diameter was studied. Blood flow changes in response to phenylephrine (αl-adrenoceptor agonist) in CFA-treated and contralateral knee joints were observed over a 40-day period, using laser Doppler flowmetery (LDF) technique. Unilateral injection of CFA (0.2 ml) increased the diameter of injected knee at all days post-injection (p<0.001) and reached to its maximum level (49.7 ± 2%) at day 3. Then, the diameter decreased gradually but did not return to its initial value. In control animals, topical application of phenylephrine (10-13-10-17 M) to the exposed joint capsule decreased blood flow in a dose-dependent manner (11.1 ± 4.4 to 58.2 ± 4.5%, p<0.001). Unilateral injection of CFA attenuated the phenylephrine response in both ipsilateral and contralateral knees compared to the response of control animals (5.2 ± 1.6 to 48.3 ± 6.1% and 1.9 ± 2.2 to 45.3 ± 5.6 % respectively, p<0.05). The reduction persisted for three weeks after CFA injection (ipsilateral for 21 days contralateral for 30 days, p<0.001). Then, the above response returned to its normal value. To evaluate the role of nitric oxide (NO) on the observed responses, amino guanidine (inducible-NO synthase inhibitor) was injected (120 mg/kg/day, i.p.) in other groups of CFA-treated animals. Arninoguanidine potentiated (p<0.001) the vasoconstrictor response to phenylephrine in both CFA injected and contralateral knees at 7, 14 and 21 days post-injection, and the increment of knee joint diameter was also less prominent. These findings may indicate that the vasoconstrictor response to phenylephrine is decreased in chronic inflammation, and increased production of NO during chronic inflammation might be involved.
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.
Mohammad Reza Bigdeli, Sohrab Hajizadeh, Mehdi Frouzandeh, Ali Khoshbaten,
Volume 11, Issue 3 (Fall 2007)
Abstract

Introduction: Prolonged and intermittent oxygen pre-exposure is associated with protection against ischemic reperfusion (IR) injury. In the current study, attempts were made to investigate the relationship between exposure to prolonged and intermittent normobaric hyperoxia (NBHO) and expression of excitatory amino acids transporters (EAATs) and TNF-α level. Method: Rats were divided into four main experimental groups, each of 21 animals. The first two were exposed to 95% inspired NBHO 4 h/day for 6 consecutive days (intermittent NBHO) or for 24 continuous hours (prolonged NBHO). The second two groups considered as controls and were exposed to 21% oxygen in the same chamber (normobaric normoxia, NBNO). Each main group was subdivided to MCAO (middle cerebral artery occlusion), sham-operated (without MCAO) and intact (without any surgery) subgroups. After 24h, MCAO subgroups were subjected to 60 min of right MCAO. After 24 h reperfusion, neurologic deficit scores (NDS) were assessed in MCAO-operated subgroups. Immediately and 48 h after pretreatment, blood sampling were done for assessing level of serum TNF-α. The effect of intermittent and prolonged NBHO on EAATs expression level was also measured using western blotting. Result: Preconditioning with prolonged and intermittent NBHO decreased NDS and up-regulated EAAT1, EAAT2, and EAAT3, significantly. Also, oxygen exposure of prolonged and intermittent NBHO increased the level of serum TNF-α. Conclusion: Although further studies are needed to clarify the protective mechanisms OF hyperoxia, the intermittent and prolonged NBHO seems to partly exert their effects via increasing the serum level of TNF-α and upregulation of glutamate transporters. However, the intermittent NBHO seems to have appropriate effects with low toxicity.
Zahra Barabadi, Sohrab Hajizadeh, Mohammad Javan, Batool Erfani, Ali Heidarian Pour,
Volume 11, Issue 4 (Winter 2008)
Abstract

Introduction: Endothelium and smooth muscle dysfunction are the most important complications of diabetes. In type 1 diabetic patients, absence of insulin leads to vasoconstriction and lower skin blood perfusion. Release of some mediators by endothelium which is induced by insulin causes vasodilation, but the exact mechanism of insulin vasodilatory effect is not detected properly. At present study we investigated the role of NO as a vasodilator and KATP channels and their intraction in the vasodilatory effect of insulin on the skin vessles. Methods: Male wistar rats (200-250 gr) were made diabetic by streptozocin (50mg/kg, s.c). After 40 days of diabetes induction, skin blood flow was measured by Laser Doppler Flowmetry technique (LDF). Insulin, LNNA (NO blocker) and Glibenclamide (KATP blocker) infusion were made by infusion pump subcutaneousely. Results: 1- Insulin increases skin blood flow in both control and diabetic groups and this increase was significantly higher in diabetic group. 2- Insulin vasodilatory effect was decreased by LNNA. 3- The vasodilatory effect of insulin was decreased by Glibenclamide. 4- Simultaneous block of both NO and KATP was more effective. Conclusion: Insulin induces vasodilation in part by NO release and partly by activation of K ATP channels. However some interaction has been seen between both routes. Although by block of both these routes, blood flow has not been completely inhibited. So it is supposed that other factors may be involved in this effect and yet to be illucidated.
Iran Pouraboli, Sohrab Hajizadeh, Hamid Najafipour, Ali Khoshbaten, Mohammadjavad Rasaei,
Volume 12, Issue 1 (Spring 2008)
Abstract

Abstract Introduction: In this study the role of PGE2 as an important inflammatory mediator in Indomethacine and Theophylline effects on joint diameter and vascular response of chronically inflamed rat knee joint to saphenous nerve stimulation was investigated. Methods: Inflammation was induced by intraarticular injection of 0.2 ml Freund,s Complete Adjuvant (FCA) and 3, 7, 14, 21 days post injection knee joint diameter, blood flow changes to saphenous nerve stimulation and PGE2 content of joint were assessed using micrometer, laser Doppler flowmeter and enzyme immunoassay kit respectively. In another three groups, control and inflamed receiving Indomethacin or Theophylline also these variables determined. Results: After inflammation induction in rat knee joint constrictory response of joint vessels to saphenous nerve stimulation reduced but joint diameter enhanced significantly. Furthermore in inflamed rats received Theophylline both vascular response of knee joint to nerve stimulation and joint diameter decreased however, daily reception of Indomethacine had no effect on joint edema but increased constrictory response of joint vessels to nerve stimulation. Furthermore PGE2 content increased in inflamed knee joint in comparison with control (uninflamed) during two weeks but in rats receiving Indomethacine it reduced significantly on days 3, 14. Also in inflamed rats treated by Theophylline PGE2 content was significantly decreased only in day 14. Conclusion: In chronic inflammation PGE2 as an inflammatory mediator play an important role in edema and modulation of constrictory response of joint vessels to nerve stimulation. Furthermore antiedematotic effect of Theophylline also may be mediated by PGE2 through decrement of vascular permeability.
Marzeieh Hoseini, Sohrab Hajizadeh, Yaghoub Fathollahi, Mojtaba Golmohammadi, Batoul Erfani, Ali Heidarian Pour,
Volume 12, Issue 1 (Spring 2008)
Abstract

Introduction:Adenosine as a potent vasodilator has physiological role in regulation of regional cerebral blood flow (rCBF). Metod: Laser-Dِoppler flowmetry technique was used to study pial vessels blood flow responses to adenosine receptors agonists and antagonist. Male Sprague Dawley rats (250-350g) that were housed in standard conditions, were anesthetized with Urethane (1.5g/kg). Adenosine (general agonist), NECA (A2Aand A2B receptor agonist) and CGS-21380(A2Aselective agonist), were used in absence and presence of A2A receptors- selective antagonist, ZM-243185, in naive and morphine-dependent rats. Results: Adenosine, NECA and CGS-21680 increased pial vessels blood flow in naive and dependent rats dose dependently. These responses were blocked significantly by ZM-243185. Responses of pial vessels to adenosine (10-4, 10-5, 10-6 M) and NECA (10-4, 10-5, 10-6 M) were increased significantly in morphine- dependent rats in comparison to naive rats. Pial vessels responses to CGS-21680 had not shown any significant deferences between morphine- dependent and naive rats. Conclusion:Based on these results it could be concluded that the role of A2B receptors in regulation of rCBF in morphine-dependent rats is more effective than A2A receptors.
Khalil Pourkhalili, Sohrab Hajizadeh, Ali Khoshbaten, Taki Tiraihi,
Volume 12, Issue 2 (Summer 2008)
Abstract

Abstract Introduction: Resent studies have been shown beneficial effects of hyperoxia pretreatment against ischemia-reperfusion injury in different organs. The aim of the present study was to investigate early and late effects of normobaric hyperoxia (≥95% O2) pretreatment on ischemia-reperfusion injuries in isolated rat hearts. Methods: Following 60 and 180 minutes of hyperoxia, rat hearts were isolated immediately (H60 and H180) or 24 hours later (H60/24 and H180/24), and subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Incidence and severity of ventricular arrhythmias, mechanical function of the heart and coronary flow were assessed during 120 min of reperfusion. LDH and CK release and infarct size were also assessed. Results: Incidence and severity of reperfusion arrhythmias significantly reduced by hyperoxia pretreatment, especially in the early phase of treanment. H180 reduced the incidence of ventricular fibrillation (VF) to 0% vs. 50% of normoxic control, p<0.05). VF duration decreased in H180 group (0 vs. 50±31s in the NC group, p<0.05) and duration of VT decreased in H60 and H180 groups compared to normoxic control group (NC) (1.5±0.7 s and 7.5±2.5 s vs. 17.7±3.3 s respectively, p<0.05). Hyperoxia improves mycardial contractile function and improves coronary flow during reperfusion. Infarct size and enzymes release were also significantly decreased in early and late phase of hyperoxia pretreatment. Conclusions: These results indicate that hyperoxia pretreatment before induction of regional heart ischemia reduces cardiac infarct size and attenuates reperfusion induced arrhythmias in isolated rat heart. Keywords: Hyperoxia, Ischemia-reperfusion injury, Heart protection, Arrhythmias
Sohrab Hajizadeh, Batool Erfani, S. Mohammad Faghihi, Zahra Barabadi, Marzeieh Hosseini,
Volume 12, Issue 3 (Fall 2008)
Abstract

Beta-2 adrenoceptors in blood vessels are one of the active factors that play a role in regulation of tissue blood flow. in diabetic angiopathy, responsiveness of these receptors is decreased, while that is increased in inflammation. According to these opposite effects, the aim of this study was to investigate the vasodilatory response of knee joint blood vessels to salbutamol (Beta-2 adrenoceptor agonist) in IDDM with combination of acute inflammation. Acute knee joint inflammation was induced by intraarticular injection of kaolin 4% and induction of diabetes was performed by streptozotocine (55 mg/kg). Wistar rats weighting 200-300 gr were used. The animals divided in 5 groups as: the control, saline, diabetic, inflammatory and diabetic- inflammatory. Blood flow of knee joint was measured using Laser Doppler Flowmeter Technique (LDF). Vasodilatation of articular micro vascular was measured in response to topical application of different concentration (10 -11 -10 -1) of salbutamol. Results obtained in this study showed that: 1- Increased knee joint diameter and perimeter due to acute inflammation in diabetic rat knee joint were significantly lesser than that of inflammatory rats. 2- Responsiveness of Beta-2 adrenoceptors were increased in kaolin- induced acute inflammation. 3- In diabetic rats, kaolin- induced acute inflammation could not increase the responsiveness of Beta-2 adrenoceptors. Based on above mentioned results, we conclude that diabetes inhibits the increasing effects of acute inflammation on responsiveness of Beta-2 adrenoceptors.
Mojtaba Golmohammadi, Sohrab Hajizadeh, Mohammad Faghihi, Marzeieh Hosein, Kambiz Rohampour,
Volume 13, Issue 2 (Summer 2009)
Abstract

Introduction: In recent study both endothelium-dependent and endothelium-independent mechanisms have been reported for the action of β-adrenoceptor. The aim of this study was to investigate on the role of nitric oxide (NO) and cyclic guanosin monophosphate (cGMP) in vasodilation mechanisms of β2-adrenoceptors (β2-AR) in rat skin vessels. Methods: All drugs were injected subcutaneous into planar skin of hind paw. Injection volume was 10µl (5µl/min). Induction of anesthesia was perform with urethane 1.5 g/kg. Laser Doppler Flowmetery (LDF) technique was used for skin blood flow (SBF) monitoring. Results: The results obtained in this study showed that different doses of salbutamol, selective β2-AR agonist (1µM) caused a significant increase of SBF, but there was not any significant different in the response of different doses. Atenolol, selective β1-adrenoceptor antagonist (10µM) alone and with salbutamol had no significant effect on SBF. Propranolol, non selective β-adrenoceptor antagonist (1µM) by itself did not changed SBF, but significantly reduced the vasodilatory effect of salbutamol. LNNA, NO inhibitor (10µM) and methylen blue, cGMP inhibitor (3µM) caused a significant decrease of SBF 6/95% and 7/91% respectively. Salbutamol injection after LNNA and NO raised the SBF to 24/7% and 22.5% respectively, which shows a significant reduction in comparison to salbutamol’s effect (42.73%). Conclusion: The results indicated that, salbutamol dilate rat skin vessels via β2- ARs. NO and cGMP involved in β2-ARs mediated vasodilation and contribute to regulation of vascular skin tone. To elucidate the exact mechanism of this response more studies are needed.
Masoumeh Sabetkasaei, Amin Ataie, Abbas Haghparast, Akbar Hajizadeh Moghaddam, Ramin Ataie, Shiva Nasiraei,
Volume 13, Issue 3 (Fall 2009)
Abstract

Introduction: Aging is the major risk factor for neurodegenerative diseases and oxidative stress is involved in the pathophysiology of these diseases. Oxidative stress can induce neuronal damages and modulate intracellular signaling, ultimately leading to neuronal death by apoptosis or necrosis. Methods: In this study, we investigated the possible antioxidant and neuroprotective properties of the polyphenolic antioxidant compound, Curcumin against homocysteine (Hcy) neurotoxicity. Curcumin (5, 15, 45 mg/kg) was injected intraperitonealy once daily for a period of 10 days beginning 5 days prior to Hcy (0.2 μmol/μl) intracerebroventricular injection in rats. Biochemical and behavioral studies, including passive avoidance learning and locomotor activity tests were studied 24 h after the last curcumin or its vehicle injection. Also Histopathological studies and cell dencity in different regions of hippocampus was investigated. Results: Hcy could induce lipid peroxidation and increase MDA and SOA levels in rats' brain. Additionally, Hcy impaired memory retention in passive avoidance learning test. However, Curcumin treatment decreased MDA and SOA levels significantly as well as improved learning and memory in rats. Histopathological analysis also indicated that Hcy could decrease hippocampus cell count and Curcumin inhibited this toxic effect. Conclusion: These results suggest that Hcy may induce lipid peroxidation in rats' brain and decrease hippocampus cells. Also polyphenol treatment (Curcumin) has the ability to improve learning and memory deficits by protecting the nervous system against Oxidative stress. Keywords: Homocysteine, Curcumin, Lipid peroxidation, Oxidative Stress
Mohammad Khaksari Hadad, Zahra Soltani, Ali Reza Sarkaki, Gholamreza Sepehri, Sohrab Hajizadeh, Abdoreza Sabahi,
Volume 14, Issue 3 (Fall 2010)
Abstract

Introduction: Following a traumatic brain injury (TBI), the excessive release of proinflammatory cytokines is major cause of cerebral edema that can cause permanent neuronal loss. This study examined the changes in brain concentrations of proinflammatory cytokines IL-1, IL-6, TNF-α and TGF- after different doses of estrogen or progesterone treatment in brain-injured rats at 6 and 24 h post-injury. Methods: Adult female rats were divided into 14 groups, and underwent either bilateral ovariectomy (12 groups) or sham surgery (2 groups). The hormones or vehicle were given intraperitoneally 0.5 h after TBI. Moderate TBI was induced by Marmarou method in TBI or treatment groups and brain levels of proinflammatory cytokines were measured 6 and 24 h post-injury. Results: The results indicated that high dose of estrogen (E2) and low dose of progesterone (P1) increase brain levels of IL-1 6 h post-injury by 52.8% and 79.2%, respectively compared to the vehicle. By the 24th h post-injury brain IL-1 level was reduced 27.5% and 27%, respectively compared to vehicle, when estrogen low dose (E1) and E2 were administered. Progesterone high dose treatment reduced brain level of IL-6 by 45.9% at 6 h post-injury and P1 treatment reduced IL-6 level by 20.5% at 24 h post-injury when compared to the vehicle. The brain TNF-α level was reduced by 72.5% by P2 at 6 h and 48.5% by E2 at 24 h post-injury, when compared to the vehicle. In addition, TGF- level seem to be increased by E1 up to 3.37 times at 24 h post-injury compared to the vehicle. Both doses of hormones showed increased levels of TGF- at 6 h post-injury, when compared to the vehicle. Conclusion: We conclude that progesterone and estrogen may change the levels of proinflammatory cytokines in the acute or delayed phases after TBI and this may be one of the mechanisms by which hormones reduce cerebral edema.
Masoumeh Kourosh Arami, Saeed Semnanian, Mohammad Javan, Sohrab Hajizadeh, Abdolrahman Sarihi,
Volume 14, Issue 4 (Winter 2011)
Abstract

Introduction: In the present work, spontaneous postsynaptic currents were assessed to investigate the postnatal development of excitatory postsynaptic currents in locus coeruleus neurons. Methods: In this study, AMPA and NMDA receptor-mediated spontaneous synaptic currents in the neurons of locus coeruleus were assessed using whole cell voltage-clamp recording during the first three weeks. Results: The frequency and amplitude of NMDA sEPSCs and the frequency of AMPA sEPSCs were increased in the second and third postnatal weeks compared with these parameters recorded in the first postnatal week. However, the ratio of the AMPA to NMDA current frequency and amplitude was constant until the 3rd postnatal week. Conclusion: These findings suggest that a vast majority of nascent glutamatergic synapses express both functional AMPA and NMDA receptors in the postnatal locus coeruleus, so that AMPA/NMDA sEPSCs remained constant during this period.
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.
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.
Morteza Gholami, Akbar Hajizadeh Moghaddam,
Volume 16, Issue 3 (Fall 2012)
Abstract

Introduction: Several studies have reported anti-anxiety effects of morphine in adult rats. The present study examined the effect of chronic morphine injections in infancy and before puberty on anxiety-like behavior in immature rats. Methods: Neonate rats (n=35) were randomly chosen and divided into two groups. On postnatal days 8-14, one group received saline and the other one received morphine. On postnatal day 21, each group was divided into subgroups. These subgroups received either morphine or saline according to the type of group on postnatal days 22-28. Finally, on postnatal days 22 and 28, rate of anxiety was studied in a plus maze. Results: On day 24 after birth, morphine increased percentage of open arm time in all groups (P<0.001). This percentage on day 28 was highest for morphine groups compared with the control group (P<0.001). The number of open arm entry on day 24 after birth was significantly increased, for both groups treated with morphine (P<0.05). The greatest difference was observed on day 28 for re-treated rats with fixed dose of morphine compared to the control group (P<0.001). Locomotor activity on days 24 and 28 after birth for both groups treated with morphine was more than the other groups (P <0.05). Conclusion: Chronic morphine administration in the neonatal period caused reduced anxiety-like behavior in immature rats. Also, re-exposure to morphine at a fixed dose had an age related anti-anxiety effect that increased in older rats.
Mohsen Nasri, Ali Mohammad Alizadeh, Vahid Khori, Sohrab Hajizadeh, Saeed Khodayari,
Volume 16, Issue 4 (Winter 2013)
Abstract

Abstract Introduction: Isolated perfused heart models such as perfusion and superfusion are commonly used for mammalian heart research. However, there are several fundamental limitations in the current techniques. In perfusion model, a suitable cannula is connected to the aorta and the perfusion is retrogradely performed. But, electrode displacement is a potential unwanted event resulted from heart contractions. In superfusion model, atrioventricular node (AV) node area is completely visible and fixed in the tissue bath after appropriate preparation, but tissue ischemia is inevitable due to the absence of cell to cell nutrition. The aim of the present study was to create a novel isolated dual perfusion/superfusion model to be used in heart physiological and pharmacological studies. Methods: The rabbit hearts (n=10) were excised. After preparation of proper sections, the electrodes were attached till the steady state appeared. The stimulation protocols consisting Wenckebach and recovery were then carried out during the isolated dual perfusion/superfusion as well as perfusion and superfusion models. Results: The AV node conduction time was increased from 33±4 ms in the isolated dual perfusion/superfusion heart model to 43±5 and 52±5 ms in perfusion and superfusion models, respectively (P<0.05). In addition, Wenckebach cycle length, effective and functional refractory periods were increased in perfusion and superfusion models compared to the isolated dual perfusion/superfusion model (P<0.05). Conclusion: This study shows the superiority of the isolated dual perfusion/superfusion heart model in tissue nutrition compared to the other common methods of mammalian heart studies.
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.
Shahram Shahmohamadi, Akbar Hajizadeh Moghaddam, Maryam Khosravi,
Volume 17, Issue 2 (Summer 2013)
Abstract

Introduction: Oxidative stress is the result of imbalance between free radicals and the antioxidant defense mechanisms of the body. Oxidative stress in brain causes dysfunction of brain activities, destruction of neurons, and disorders like Alzheimer disease. In this experimental study, we examined the protective effect of Salvia officinalis L. against oxidative stress induced by intracerebroventricular injection of streptozotocin in male rats. Methods: In the experimental research, Wistar rats were divided into control, sham, and experimental groups. Experimental groups received 25, 50 and 100 mg/kg body weight of hydroalcoholic extract of Salvia officinalis intraperitoneally. After two weeks, surgical procedure was performed on sham and experimental groups and after one week of recovery, streptozotocin was injected intracerebroventricularly (i.c.v-STZ) at 3 mg/kg. Brain hemispheres were separated after four weeks. Finally, superoxide dismutase (SOD) and catalase (CAT) levels were measured in brain hemispheres. Results: In the group receiving STZ, CAT and SOD levels were significantly decreased compared to the control group (P<0.001), whereas intraperitoneal injection of different doses of Salvia officinalis leaves extract significantly increased SOD and CAT levels compared to STZ group (P<0.001). Conclusion: These data show that antioxidant effects of Salvia officinalis L. could prevent oxidative stress induced by i.c.v.-STZ injection in the brains of male rats.

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