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Showing 7 results for Khosravi

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.
Fatemeh Jafari, Maryam Khosravi, Akram Najafi-Abedi, Hedayat Sahraei, Mina Ranjbaran, Nasrin Amooei, Cyrus Jalili, Maryam Bagherpour,
Volume 17, Issue 2 (Summer 2013)
Abstract

Introduction: Rosa Damasca essential oil is currently used as anti-depressant in animal models and human. Considering the similarities between Rosa Canina and Rosa Damasca, the effects of water and alcoholic extracts of R. Canina on depression induced by forced swimming test (FST) in mice were investigated. Methods: Male NMRI mice (25-30 g) were used (n=6/group). Intraperitoneal injections of alcoholic (5, 10, 20, 30, and 40 mg/kg) and/or water (10, 20 and 30 mg/kg) extracts were administered to the animals 30 min before the FS. Intracerebroventricular injections of the alcoholic and water extracts (1, 5 and 10 μg/mice) to the animals were performed 5 min before FST. Results: Both intraperitoneal (20 and 30 mg/kg) and intracerebroventricular (5, 10 μg/Mouse) injections of R. Canina L. water extract dose-dependently reduced the animals immobilization, which was similar to the fluoxetine effect. However, the alcoholic extract of R. Canina L. did not change the immobility time in the animals when used intraperitoneally and intracerebroventricularly. Conclusion: It could be concluded that the water extract of R.Canina can inhibit depression induced by FST in mice. Since there are some components in the extract that can interact with D2 dopamine receptors in the brain, it is likely that the extract induced its antidepressant effects via such mechanism.
Mina Ranjbaran, Shohreh Javadzadeh, Maryam Khosravi, Hassan Ghoshooni, Seyedeh Maedeh Fatemi, Jamal Shams, Hedayat Sahraei,
Volume 17, Issue 4 (Winter 2014)
Abstract

Introduction: Topiramate is an anti-convulsant drug, which produces its effects via glutamate metabotropic receptors inhibition and/or GABA receptor excitation. In the present study, attempts were made to investigate the effects of topiramate on the tolerance to morphine-induced analgesia activity in male NMRI mice (20-30 g). Methods: Hot plate method was chosen for the study. First of all the analgesic effects of morphine and topiramate on mice were investigated. Then, the animals became tolerant to morphine (50 mg/kg twice daily for three consecutive days). Different doses of topiramate were administered to the animals 30 min before each morphine (50 mg/kg) injections (acquisition) during tolerance development or on the test day, 30 min before the experiment. Results: Subcutaneous morphine injection (10 mg/kg) induced analgesia. However, intraperitoneal administration of topiramate (0.5, 2.5 and 5 mg/kg) had no effect. In addition, topiramate (0.5, 2.5 and 5 mg/kg) did not affect morphine-induced analgesia. Administration of a single daily dose of morphine (50 mg/kg twice daily) for 3 days, induced tolerance. Injections of topiramate (0.5 and 2.5 mg/kg) had no effects on the acquisition of morphine tolerance. However, topiramate (0.5 and 2.5 mg/kg) enhanced the expression of morphine tolerance. The drug reduced the expression of morphine tolerance at the dose of 5 mg/kg. Conclusion: Topirmate showed a biphasic effect on the expression of tolerance to morphine-induced analgesia in lower and higher doses which may be due to glutamate and/or GABAergic mechanisms.
Gholamreza Bagheri Nikoo, Maryam Khosravi, Hedayat Sahraei, Mina Ranjbaran, Nahid Sarahian, Homeira Zardooz, Zahra Bourbour, Maryam Alemaref, Gila Pirzad Jhromi, Gholamreza Herfehdoost,
Volume 18, Issue 1 (Spring 2014)
Abstract

Introduction: The brain glutamate system plays a central role in response to stress. This study examines the effect of memantine (a NMDA glutamate receptor antagonist) on stress from plantar electrical shock in male NMRI mice (Pasture Institute, Iran), weighing 25-30 g (n=6/group). Methods: The nucleus accumbens was bilaterally cannulated in a group of animals, and seven days later, different doses of memantine (1 and 5 μg/mouse) was administered 5 min before inducing stress. In other groups, different doses of the drug (1 and 5 mg/kg) were administered to the animals intraperitoneally 30 min before the stress induction. Then food and water intake, anorexia, and the amount of urine and fecal materials were measured. Results: The stress reduced food intake and increased water intake in the animals. In addition, anorexia, fecal weight and urine volume were increased dramatically in these animals. Intraperitoneal memantine injection increased food intake and decreased water intake. This occurred when the drug was administered intra-accumbally, too. Memantine inhibited stress-induced anorexia when administered either intraperitoneally or intra-accumbally. Memantine (both peripherally and centrally) also changed stress-induced fecal passage but decreased urination. Conclusion: Memantine administration can inhibit or potentiate stress effects, which may be at least partially integrated in the nucleus accumbens.
Mahboubeh Kamali, Hedayat Sahraei, Maryam Khosravi, Shahin Hassanpour, Habib Yaribeygi,
Volume 19, Issue 4 (December 2015)
Abstract

Introduction: Morphine withdrawal syndrome is mediated via several central and peripheral neurological pathways. In the present study we investigated the role of N-methyl-D aspartic acid (NMDA) glutamate receptor on naloxone-induced withdrawal syndrome in morphine-conditioned mice. Materials and Methods: We designed two separate experiments. In experiment one, 30 male NMRI mice were divided into 5 groups, pretreated with memantine (0.1, 1 and 5 mg/kg; I.P.) followed by morphine-dependence period for 3 days. In the other experiment, 48 male NMRI mice distributed into 8 groups, pretreated with intra-accumbens (IAc) memantine (1 and 5 μg/animal) within the right, left and both side of nucleus accumbens (RNAcc, LNAcc and BNAcc) followed by I.P. morphine-dependence (3 days). On day 4, in both experiments, morphine was injected into mice, followed by naloxone. Then naloxone-induced total jumping count, jump height and defecation in morphine-conditioned mice were recorded for 30 min. Results: Pre-treatment by I.P. injection of memantine significantly attenuated naloxone precipitated jumping count/30 min, jumping height (mm) and fecal material output in morphine dependent mice (P<0.05). Also, IAC pretreatment with memantine in LNAcc, RNAcc and BNAcc significantly declined the effect of I.P. injection of naloxone on total jumping count and jumping height (P<0.05), pretreatment within memantine in LNAcc, RNAcc and BNAcc had no effect on defecation (P>0.05). Conclusion: These findings indicated asymmetric involvement of central and peripheral NMDA glutamate receptors in withdrawal syndrome development in morphine-dependent mice.


Pedram Torabian, Ayyoob Khosravi, Mehdi Gholizadeh, Mehdi Zahedi, Majid Haghjoo, Morteza Oladnabi, Yahya Jand, Vahid Khori,
Volume 20, Issue 3 (September 2016)
Abstract

Introduction: Congenital long QT syndrome (LQTS) is a cardiac disorder characterized by QT interval prolongation at basal ECG. Different LQTS genes encode ion channel subunits or proteins involved in regulating cardiac ionic currents. Long QT syndrome type 6 (LQT6) is caused by mutation in the KCNE2 gene. Our research aimed to analyze genetic variants of KCNE2 gene causing the disease in Iranian population. Methods: Twenty nine patients consented for participation in the study. They were diagnosed based on Schwartz's criteria. After DNA extraction from peripheral blood cells, two exons of the KCNE2 gene were amplified. Afterwards, PCR-SSCP was carried out for screening the possible mutated gene variants. As the last verification step, direct sequencing was done to determine the sequence. Results: All samples were detected by PCR-SSCP and sequenced. None of the patients had the mutation in the KCNE2 gene. Conclusion: Investigating a genetic variant associated with LQTS, in Iranian patients clinically diagnosed with LQT6, no association was found between the disease and KCNE2 gene. Other previously identified genes, especially the major genes, should be considered for further investigation.


Alireza Samimiat, Mohammad Sedigh Khosravi, Jalal Hassanshahi, Mehdi Nematbakhsh,
Volume 22, Issue 2 (June 2018)
Abstract

Introduction: Renal ischemia-reperfusion (RIR) may disturb renin-angiotensin system components. In this study, the effects of Mas receptor (A779) and AT2 receptor (PD123319) antagonists were examined in RIR rats. Methods: Total 60 male and female Wistar rats were assigned into 10 groups (n=6 in each group), including sham-operated group, RIR groups treated with the vehicle, A779, PD123319, or A779+PD123319. The rats were subjected to 30 minutes renal ischemia followed by 75 minutes reperfusion and the vehicle/antagonists were started to infuse 15 minutes after beginning of reperfusion for 60 min. Mean arterial pressure (MAP) and renal perfusion pressure responses to antagonists were assessed. Measurements for kidney function parameters also were performed. All the measurements were made at the end of 60 min vehicle/antagonist infusion. Results: MAP has altered significantly during RIR times (P=0.004), but no significant difference was observed between two genders. The RIR itself in injured rats (compared to sham operated rats) decreased urine flow (UF), creatinine clearance (Ccr), filtrate load of sodium (FNa) and sodium excretion rate (ENa) significantly in both genders (P<0.05). The antagonists infusion caused significant decrease in Ccr and FNa in male and female rats subjected to RIR when compared with vehicle (P<0.05), but the UF decreased significantly (P<0.05) only in PD123319 treated groups; however, there was no significant difference in ENa between the RIR groups in both genders. Conclusion: Our findings showed the importance role of Mas receptor and AT2 receptor on renal function after kidney ischemia/reperfusion in RIR rat model.



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