Sara Soleimani Asl | Hamadan Medical sciences University (original) (raw)

Papers by Sara Soleimani Asl

Research paper thumbnail of Vitamin C Can Alter Lead-Induced Passive Avoidance Learning Impairment in Rats

She teaches goss anatomy, histology, and embryology and her research interests are drug addiction... more She teaches goss anatomy, histology, and embryology and her research interests are drug addiction and memory. Introduction: Lead (Pb) is a neurotoxin that its different effects on the central nervous system are well-known. Previous studies have reported the potent effects of vitamin C on memory. The present study was undertaken to evaluate the protective effects of vitamin C against lead-induced amnesia. Methods: Male Wistar rats were divided into 4 groups: the control (saline), negative control (lead), positive control (Vitamin C, 150 mg/kg), and experimental (Lead+Vitamin C). To induce lead toxicity, the rats received water containing 0.2% Pb instead of regular water for 1 month. Passive avoidance learning was assessed by Shuttle Box 2 months later. Retention was tested 24 hours after training. Results: The results showed that lead causes impairment in acquisition and retrieval processes of passive avoidance learning and memory. However, vitamin C administration reinforced passive avoidance learning and memory. All results were significant (P<0.001). Conclusion: Vitamin C administration in rats counteracts the negative effect of lead on spatial learning and memory.

Research paper thumbnail of Protective Effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-Induced Neurotoxicity in Cerebellum of Male Rats

Autonomic Neuroscience Basic Clinical, Sep 1, 2011

Introduction: 3-4, methylenedioxymethamphetamine (MDMA) causes apoptosis in nervous system and se... more Introduction: 3-4, methylenedioxymethamphetamine (MDMA) causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein (NAC) as an antioxidant on MDMAinduced apoptosis. Methods: 21 Sprague dawley male rats (200-250mg) were treated with MDMA (2×0,5mg/kg) or MDMA plus NAC (100mg/kg IP for 7 day). After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method.

Research paper thumbnail of A Decrease of Reelin Expression in Neonatal Ventral Hippocampal Lesion Model of Schizophrenia

Journal of Applied Biotechnology Reports, Sep 15, 2014

ABSTRACT Schizophrenia affects 1% of population. Neonatal ventral hippocampus lesion (NVHL) model... more ABSTRACT Schizophrenia affects 1% of population. Neonatal ventral hippocampus lesion (NVHL) model of schizophrenia designed in 1993 by Lipska is a widely studied developmental animal model of schizophrenia. NVHL rats mimic many of the symptoms of schizophrenia in detail. We studied this model in molecular level and reelin expression in it. Reelin is an extracellular matrix glycoprotein that regulates some processes in CNS development and reduces significantly in schizophrenia. For this study, animals (male pups) take into 3 groups: control, sham and experiment. The lesion made by injection of 0.3 μl. Isotonic Neurotoxin with stereotaxic surgery in age 7 day and body weight 11-15 gr. Social behavioral and stereotypic movement assessed in age 56 day then reelin expression in frontal cortex was evaluated by western blotting. Behavioral analysis and histological studies demonstrated the schizophrenia model. Western blotting of reelin protein in frontal cortex and hippocampus showed a decrease of reelin (P value: 0.012) in experimental group as compared to control and sham group. So, in the NVHL as a common and more similar model of schizophrenia reelin expression significantly decreases in frontal cortex and hippocampus that means this model in molecular pathways is similar to the disease.

Research paper thumbnail of The Effect of TGF-alpha on Neurogenesis in Subventricular Zone of Rat Brain after Ischemia-Reperfusion

Stroke is the third important reason of death in adults and an important cause of adult disabilit... more Stroke is the third important reason of death in adults and an important cause of adult disability. Previous studies suggest that TGF-alpha can induce neurogenesis after stroke. Here in, we studied neurogenesis effects of the TGF-alpha on subventricular zone following ischemia-reperfusion. Methods: Male wistar rats (250-300 g) were divided into ischemia and treatment groups. After induction of ischemia-reperfusions, PBS (phosphate buffer salin) and TGF-alpha 50 ng were injected stereotaxicaly in lateral ventricle in ischemia and treatment respectively. After 12 days, the nestin expression in subventricular zone was assessed by immunohistochemical staining method. Results: Our results showed that nestin expression increased significantly in treatment group in comparison with ischemia group (p<0.05) . Discussion: Expression of nestin in SVZ indicates that TGF-α can stimulate the neural stem cells proliferation after ischemia -reperfusion injury.

Research paper thumbnail of N-acetylcysteine can alter 3,4-methylenedioxymethamphetamine-induced apoptosis in hippocampi of male rats

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2015

Research paper thumbnail of Effect of Amyloid β- Peptide on Passive Avoidance Learning in Rats: A Behavioral Study

Avicenna Journal of Neuro Psych Physiology, 2014

Research paper thumbnail of Effects of nitric oxide on the prefrontal cortex in stressed rats

BACKGROUND: Nitric oxide (NO) exhibits both protective and detrimental effects in the central ner... more BACKGROUND: Nitric oxide (NO) exhibits both protective and detrimental effects in the central nervous system. OBJECTIVE: To investigate the effect of NO on the prefrontal cortex in neonatal stressed rats. DESIGN, TIME AND SETTING: A randomized, controlled, animal study was performed at the METHODS: Rat stress models were established by immobilization and randomly received intraperitoneal injection of 2 mL physiological saline, L-arginine (200 mg/kg) as a NO precursor, N(G)-nitro-L-arginine methyl ester (20 mg/kg), or subcutaneous injection of 7-nitroindazole (25 mg/kg) as a NO synthase inhibitor. MAIN OUTCOME MEASURES: After the rats were treated for 4 weeks, the frontal cortex was harvested for histological observation and NO detection. RESULTS: Subcutaneous administration of N(G)-nitro-L-arginine methyl ester or 7-nitroindazole resulted in significantly lower prefrontal cortex thickness and NO production compared with subcutaneous administration of L-arginine (P < 0.05). Prefrontal cortex thickness significantly increased in rats following L-arginine treatment, compared with physiological saline intervention ( P < 0.05). CONCLUSION: NO exhibited protective effects on the prefrontal cortex of stressed rats.

Research paper thumbnail of Reduction in ischemic brain injury following the administration of pentoxifylline after transient global ischemia/ reperfusion in a rat model

Medical journal of the Islamic Republic of Iran, 2015

It is well known that the hippocampus, the CA1 Pyramidal cells in particular, is selectively vuln... more It is well known that the hippocampus, the CA1 Pyramidal cells in particular, is selectively vulnerable during global cerebral ischemia. Recently, it is observed that pentoxifylline has a neuroprotective effect. This study explored the pharmacological relationship between ischemiainduced cell death of the hippocampus and the efficacy of a vasodilator agent (pentoxifylline) in the prevention of delayed neuronal death. This experimental study was performed on 4 groups: control, ischemia, experimental (200mg/kg pentoxifylline injection one hour prior to and one hour following ischemia) and vehicle (normal saline). Transient global ischemia was induced by bilateral common carotid arteries occlusion. To investigate the apoptotic bodies and caspase-3 activities as a central role in the execution phase of apoptosis, the brains were prepared for the TUNEL technique. Pentoxifylline administration limited apoptosis and caspase-3 activities in rats' hippocampi. Our data showed no significa...

Research paper thumbnail of Acute and Chronic Effects of 3-4, Methylenedioxymethamphetamine on Pyramidal Cells of Hippocampus

Avicenna Journal of Neuro Psych Physiology, 2014

Research paper thumbnail of Protective Effect of Vitamin E Against Lead-induced Memory and Learning Impairment in Male Rats

Avicenna Journal of Neuro Psych Physiology, 2015

Research paper thumbnail of Sex differences in MDMA-induced toxicity in Sprague-Dawley rats

Functional neurology, Jan 6, 2015

Recent evidence demonstrates that female subjects show exaggerated responses to 3,4-methylenediox... more Recent evidence demonstrates that female subjects show exaggerated responses to 3,4-methylenedioxymethamphetamine (MDMA) compared with males. The aim of our study was to evaluate sex differences and the role of endogenous gonadal hormones on the effects of MDMA. Fifty-six intact and gonadectomized male and female Sprague-Dawley rats were randomly assigned to either MDMA (5 mg/kg) or saline treatment. Learning and memory were assessed using the Morris water maze (MWM). The expression of Bax and Bcl-2 in the hippocampus was detected by Western blotting. Behavioral analysis showed that MDMA led to memory impairment in both male and female rats. The female rats showed more sensitivity to impairment than the males, as assessed using all the memory parameters in the MWM. Ovariectomy attenuated the MDMA-induced memory impairment. By contrast, orchiectomized rats showed more impairment than MDMA-treated intact male rats. Bcl-2 and Bax were down-regulated and up-regulated in MDMA-treated mal...

Research paper thumbnail of Acute Effects of Ecstasy on Memory Are more Extensive than Chronic Effects

Basic and clinical neuroscience, 2014

Exposure to 3, 4- methylenedioxymethamphetamine (MDMA) could lead to serotonergic system toxicity... more Exposure to 3, 4- methylenedioxymethamphetamine (MDMA) could lead to serotonergic system toxicity in the brain. This system is responsible for learning and memory functions. Studies show that MDMA causes memory impairment dose-dependently and acutely. The present study was designed to evaluate the chronic and acute effects of MDMD on spatial memory and acquisition of passive avoidance. Adult male Wistar rats (200-250 g) were given single or multiple injections of MDMA (10 mg/kg, IP). Using passive avoidance and Morris Water Maze (MWM) tasks, learning and spatial memory functions were assessed. The data were analyzed by SPSS 16 software and one- way analysis of variance (ANOVA) test. Our results showed that there were significant differences in latency to enter the dark compartment (STL) between sham and MDMA- treated groups. Acute group significantly showed more STL in comparison with chronic group. Furthermore, MDMA groups spent more time in dark compartment (TDS) than the sham gro...

Research paper thumbnail of Ecstasy-induced caspase expression alters following ginger treatment

Basic and clinical neuroscience, 2013

Exposure to 3-4, methylenedioxymethamphetamine (MDMA) leads to cell death. Herein, we studied the... more Exposure to 3-4, methylenedioxymethamphetamine (MDMA) leads to cell death. Herein, we studied the protective effects of ginger on MDMA- induced apoptosis. 15 Sprague dawley male rats were administrated with 0, 10 mg/kg MDMA, or MDMA along with 100mg/kg ginger, IP for 7 days. Brains were removed to study the caspase 3, 8, and 9 expressions in the hippocampus by RT-PCR. Data was analyzed by SPSS 16 software using the one-way ANOVA test. MDMA treatment resulted in a significant increase in caspase 3, 8, and 9 as compared to the sham group (p < 0.001). Ginger administration however, appeared to significantly decrease the same (p < 0.001). Our findings suggest that ginger consumption may lead to the improvement of MDMA-induced neurotoxicity.

Research paper thumbnail of Transforming Growth Factor-α Improves Memory Impairment and Neurogenesis Following Ischemia Reperfusion

Cell journal, 2014

Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ven... more Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ventricular zone neurons are vulnerable to ischemia that can impair memory and learning functions. Although neurogenesis normally occurs in the dentate gyrus (DG) of the hippocampus and sub-ventricular zone (SVZ) following brain damage, this response is unable to compensate for severely damaged areas. This study aims to assess both neurogenesis and the neuroprotective effects of transforming growth factor-alpha (TGF-α) on the hippocampus and SVZ following ischemia-reperfusion. In this experimental study, a total of 48 male Wistar rats were divided into the following groups: surgical (n=12), phosphate buffered saline (PBS) treated vehicle shams (n=12), ischemia (n=12) and treatment (n=12) groups. Ischemia was induced by common carotid occlusion for 30 minutes followed by reperfusion, and TGF-α was then injected into the right lateral ventricle. Spatial memory was assessed using Morris water ...

Research paper thumbnail of Evaluation of Bcl-2 Family Gene Expression in Hippocampus of 3, 4-methylenedioxymethamphetamine Treated Rats

Cell journal, 2012

3,4-methylenedioxymethamphetamine (MDMA) is an illicit, recreational drug that causes cellular de... more 3,4-methylenedioxymethamphetamine (MDMA) is an illicit, recreational drug that causes cellular death and neurotoxicity. This study evaluates the effects of different doses of MDMA on the expression of apoptosis-related proteins and genes in the hippocampus of adult rats. In this expremental study,a total of 20 male Sprague Dawley rats (200-250 g ) were treated with MDMA (0, 5, 10, 20 mg/kg i.p. twice daily) for 7 days. Seven days after the last administration of MDMA, the rats were killed. Bax and Bcl-2 genes in addition to protein expressions were detected by western blot and reverse transcriptionpolymerase chain reaction (RT-PCR).Results were analyzed using one-way ANOVA and p≤0.05 was considered statistically significant. Our results showed that MDMA caused dose dependent up-regulation of Bax and down-regulation of Bcl-2 in the hippocampus. There was a significant alteration in bcl-2 and bax genes density. Changes in apoptosis-related proteins and respective genes relating to Bax...

Research paper thumbnail of Protective Effects of Borago officinalis Extract on Amyloid β-Peptide(25–35)-Induced Memory Impairment in Male Rats: A Behavioral Study

BioMed Research International, 2014

Research paper thumbnail of The protective effect of Borago Officinalis extract on amyloid β (25–35)-induced long term potentiation disruption in the dentate gyrus of male rats

Metabolic Brain Disease, 2014

Alzheimer&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disea... more Alzheimer&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease (AD) begins with impairment in synaptic functions before developing into later neurodegeneration and neural loss. In the present study we have examined the protective effects of Borago Officinalis (borage) extract on amyloid β (Aβ)--Induced long term potentiation (LTP) disruption in hippocampal dentate gyrus (DG). Wistar male rats received intrahippocampal (IHP) injection of the Aβ (25-35) and borage extract throughout gestation (100 mg/kg). LTP in perforant path- DG synapses was assessed using electrophysiology method and field excitatory post- synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured by 400 Hz tetanization. Finally, the total thiol content of hippocampus was measured using colorimetric reaction based on the Ellman&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s method. The results showed that Aβ (25-35) significantly decreased fEPSP slope and SP amplitude comparing with the control and sham group, whereas borage extract administration increased these parameters compared to the Aβ group. Aβ induced a remarkable decrease in total thiol content of hippocampus and borage prevented the decrease of the hippocampal total sulfhydryl (SH) groups. This data suggest that Aβ (25-35) can effectively inhibit LTP in the granular cells of the DG in hippocampus, and borage supplementation reverse the synaptic plasticity in DG following Aβ treatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.

Research paper thumbnail of Attenuation of ecstasy-induced neurotoxicity by N-acetylcysteine

Metabolic Brain Disease, 2014

Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and ... more Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and hippocampal cell death. Numerous evidence indicates that the antioxidant N-acetylcysteine (NAC) exerts protective effects in the brain. The present study evaluates the effects of NAC on MDMA-induced neurotoxicity. We intraperitoneally injected 28 adult male Sprague-Dawley rats (200-250 g) with either 0, 10 mg/kg of MDMA, or 10 mg/kg of MDMA plus 100 mg/kg of NAC. Spatial memory was assessed with a Morris Water Maze (MWM). At the end of the study, rats&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39; brains were removed to study the structure and ultrastructure of CA1, and measure Bcl-2 and Bax expressions in the hippocampus. In the MWM, NAC treatment significantly attenuated the MDMA-induced increase in distance traveled (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) and escape latency (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.001). The decreased time spent in the target quadrant in MDMA-treated animals was attenuated by NAC (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01). NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively. These data have suggested that NAC could protect against behavioral changes and apoptosis in the hippocampus following administration of MDMA. NAC might be useful for the treatment of neurotoxicity in MDMA users.

Research paper thumbnail of Protective effects of N-acetylcysteine on 3, 4-methylenedioxymethamphetamine-induced neurotoxicity in male Sprague–Dawley rats

Metabolic Brain Disease, 2013

Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hipp... more Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hippocampal cell death. In the present study we have examined the protective effects of N-acetyl-L-cysteine (NAC) on MDMA-induced neurotoxicity. A total of 56 male Sprague Dawley rats (200-250 g) received twice daily intraperitoneal (IP) injections of 5, 10 or 20 mg/kg MDMA plus NAC (100 mg/kg). Rectal temperatures were recorded before and after daily treatment. We used a Morris water maze (MWM) to assess spatial learning and memory. At the end of the study rats&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39; brains were removed, cells were counted and the level of Bcl-2, Bax and caspase-3 expression in the hippocampi were measured. NAC pretreatment significantly reduced MDMA-induced hyperthermia. In the MWM, NAC significantly attenuated the MDMA-induced increase in distance traveled; however the observed increase in escape latency was not significant. The decrease in time spent in the target quadrant in MDMA animals was significantly attenuated (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.001, all groups). NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2. This data suggested a possible benefit of NAC in the treatment of neurotoxicity among those who use MDMA.

Research paper thumbnail of Zingiber officinale alters 3,4-methylenedioxymethamphetamine-/INS;induced neurotoxicity in rat brain

Journal of the Neurological Sciences, 2013

Research paper thumbnail of Vitamin C Can Alter Lead-Induced Passive Avoidance Learning Impairment in Rats

She teaches goss anatomy, histology, and embryology and her research interests are drug addiction... more She teaches goss anatomy, histology, and embryology and her research interests are drug addiction and memory. Introduction: Lead (Pb) is a neurotoxin that its different effects on the central nervous system are well-known. Previous studies have reported the potent effects of vitamin C on memory. The present study was undertaken to evaluate the protective effects of vitamin C against lead-induced amnesia. Methods: Male Wistar rats were divided into 4 groups: the control (saline), negative control (lead), positive control (Vitamin C, 150 mg/kg), and experimental (Lead+Vitamin C). To induce lead toxicity, the rats received water containing 0.2% Pb instead of regular water for 1 month. Passive avoidance learning was assessed by Shuttle Box 2 months later. Retention was tested 24 hours after training. Results: The results showed that lead causes impairment in acquisition and retrieval processes of passive avoidance learning and memory. However, vitamin C administration reinforced passive avoidance learning and memory. All results were significant (P<0.001). Conclusion: Vitamin C administration in rats counteracts the negative effect of lead on spatial learning and memory.

Research paper thumbnail of Protective Effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-Induced Neurotoxicity in Cerebellum of Male Rats

Autonomic Neuroscience Basic Clinical, Sep 1, 2011

Introduction: 3-4, methylenedioxymethamphetamine (MDMA) causes apoptosis in nervous system and se... more Introduction: 3-4, methylenedioxymethamphetamine (MDMA) causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein (NAC) as an antioxidant on MDMAinduced apoptosis. Methods: 21 Sprague dawley male rats (200-250mg) were treated with MDMA (2×0,5mg/kg) or MDMA plus NAC (100mg/kg IP for 7 day). After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method.

Research paper thumbnail of A Decrease of Reelin Expression in Neonatal Ventral Hippocampal Lesion Model of Schizophrenia

Journal of Applied Biotechnology Reports, Sep 15, 2014

ABSTRACT Schizophrenia affects 1% of population. Neonatal ventral hippocampus lesion (NVHL) model... more ABSTRACT Schizophrenia affects 1% of population. Neonatal ventral hippocampus lesion (NVHL) model of schizophrenia designed in 1993 by Lipska is a widely studied developmental animal model of schizophrenia. NVHL rats mimic many of the symptoms of schizophrenia in detail. We studied this model in molecular level and reelin expression in it. Reelin is an extracellular matrix glycoprotein that regulates some processes in CNS development and reduces significantly in schizophrenia. For this study, animals (male pups) take into 3 groups: control, sham and experiment. The lesion made by injection of 0.3 μl. Isotonic Neurotoxin with stereotaxic surgery in age 7 day and body weight 11-15 gr. Social behavioral and stereotypic movement assessed in age 56 day then reelin expression in frontal cortex was evaluated by western blotting. Behavioral analysis and histological studies demonstrated the schizophrenia model. Western blotting of reelin protein in frontal cortex and hippocampus showed a decrease of reelin (P value: 0.012) in experimental group as compared to control and sham group. So, in the NVHL as a common and more similar model of schizophrenia reelin expression significantly decreases in frontal cortex and hippocampus that means this model in molecular pathways is similar to the disease.

Research paper thumbnail of The Effect of TGF-alpha on Neurogenesis in Subventricular Zone of Rat Brain after Ischemia-Reperfusion

Stroke is the third important reason of death in adults and an important cause of adult disabilit... more Stroke is the third important reason of death in adults and an important cause of adult disability. Previous studies suggest that TGF-alpha can induce neurogenesis after stroke. Here in, we studied neurogenesis effects of the TGF-alpha on subventricular zone following ischemia-reperfusion. Methods: Male wistar rats (250-300 g) were divided into ischemia and treatment groups. After induction of ischemia-reperfusions, PBS (phosphate buffer salin) and TGF-alpha 50 ng were injected stereotaxicaly in lateral ventricle in ischemia and treatment respectively. After 12 days, the nestin expression in subventricular zone was assessed by immunohistochemical staining method. Results: Our results showed that nestin expression increased significantly in treatment group in comparison with ischemia group (p<0.05) . Discussion: Expression of nestin in SVZ indicates that TGF-α can stimulate the neural stem cells proliferation after ischemia -reperfusion injury.

Research paper thumbnail of N-acetylcysteine can alter 3,4-methylenedioxymethamphetamine-induced apoptosis in hippocampi of male rats

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2015

Research paper thumbnail of Effect of Amyloid β- Peptide on Passive Avoidance Learning in Rats: A Behavioral Study

Avicenna Journal of Neuro Psych Physiology, 2014

Research paper thumbnail of Effects of nitric oxide on the prefrontal cortex in stressed rats

BACKGROUND: Nitric oxide (NO) exhibits both protective and detrimental effects in the central ner... more BACKGROUND: Nitric oxide (NO) exhibits both protective and detrimental effects in the central nervous system. OBJECTIVE: To investigate the effect of NO on the prefrontal cortex in neonatal stressed rats. DESIGN, TIME AND SETTING: A randomized, controlled, animal study was performed at the METHODS: Rat stress models were established by immobilization and randomly received intraperitoneal injection of 2 mL physiological saline, L-arginine (200 mg/kg) as a NO precursor, N(G)-nitro-L-arginine methyl ester (20 mg/kg), or subcutaneous injection of 7-nitroindazole (25 mg/kg) as a NO synthase inhibitor. MAIN OUTCOME MEASURES: After the rats were treated for 4 weeks, the frontal cortex was harvested for histological observation and NO detection. RESULTS: Subcutaneous administration of N(G)-nitro-L-arginine methyl ester or 7-nitroindazole resulted in significantly lower prefrontal cortex thickness and NO production compared with subcutaneous administration of L-arginine (P < 0.05). Prefrontal cortex thickness significantly increased in rats following L-arginine treatment, compared with physiological saline intervention ( P < 0.05). CONCLUSION: NO exhibited protective effects on the prefrontal cortex of stressed rats.

Research paper thumbnail of Reduction in ischemic brain injury following the administration of pentoxifylline after transient global ischemia/ reperfusion in a rat model

Medical journal of the Islamic Republic of Iran, 2015

It is well known that the hippocampus, the CA1 Pyramidal cells in particular, is selectively vuln... more It is well known that the hippocampus, the CA1 Pyramidal cells in particular, is selectively vulnerable during global cerebral ischemia. Recently, it is observed that pentoxifylline has a neuroprotective effect. This study explored the pharmacological relationship between ischemiainduced cell death of the hippocampus and the efficacy of a vasodilator agent (pentoxifylline) in the prevention of delayed neuronal death. This experimental study was performed on 4 groups: control, ischemia, experimental (200mg/kg pentoxifylline injection one hour prior to and one hour following ischemia) and vehicle (normal saline). Transient global ischemia was induced by bilateral common carotid arteries occlusion. To investigate the apoptotic bodies and caspase-3 activities as a central role in the execution phase of apoptosis, the brains were prepared for the TUNEL technique. Pentoxifylline administration limited apoptosis and caspase-3 activities in rats' hippocampi. Our data showed no significa...

Research paper thumbnail of Acute and Chronic Effects of 3-4, Methylenedioxymethamphetamine on Pyramidal Cells of Hippocampus

Avicenna Journal of Neuro Psych Physiology, 2014

Research paper thumbnail of Protective Effect of Vitamin E Against Lead-induced Memory and Learning Impairment in Male Rats

Avicenna Journal of Neuro Psych Physiology, 2015

Research paper thumbnail of Sex differences in MDMA-induced toxicity in Sprague-Dawley rats

Functional neurology, Jan 6, 2015

Recent evidence demonstrates that female subjects show exaggerated responses to 3,4-methylenediox... more Recent evidence demonstrates that female subjects show exaggerated responses to 3,4-methylenedioxymethamphetamine (MDMA) compared with males. The aim of our study was to evaluate sex differences and the role of endogenous gonadal hormones on the effects of MDMA. Fifty-six intact and gonadectomized male and female Sprague-Dawley rats were randomly assigned to either MDMA (5 mg/kg) or saline treatment. Learning and memory were assessed using the Morris water maze (MWM). The expression of Bax and Bcl-2 in the hippocampus was detected by Western blotting. Behavioral analysis showed that MDMA led to memory impairment in both male and female rats. The female rats showed more sensitivity to impairment than the males, as assessed using all the memory parameters in the MWM. Ovariectomy attenuated the MDMA-induced memory impairment. By contrast, orchiectomized rats showed more impairment than MDMA-treated intact male rats. Bcl-2 and Bax were down-regulated and up-regulated in MDMA-treated mal...

Research paper thumbnail of Acute Effects of Ecstasy on Memory Are more Extensive than Chronic Effects

Basic and clinical neuroscience, 2014

Exposure to 3, 4- methylenedioxymethamphetamine (MDMA) could lead to serotonergic system toxicity... more Exposure to 3, 4- methylenedioxymethamphetamine (MDMA) could lead to serotonergic system toxicity in the brain. This system is responsible for learning and memory functions. Studies show that MDMA causes memory impairment dose-dependently and acutely. The present study was designed to evaluate the chronic and acute effects of MDMD on spatial memory and acquisition of passive avoidance. Adult male Wistar rats (200-250 g) were given single or multiple injections of MDMA (10 mg/kg, IP). Using passive avoidance and Morris Water Maze (MWM) tasks, learning and spatial memory functions were assessed. The data were analyzed by SPSS 16 software and one- way analysis of variance (ANOVA) test. Our results showed that there were significant differences in latency to enter the dark compartment (STL) between sham and MDMA- treated groups. Acute group significantly showed more STL in comparison with chronic group. Furthermore, MDMA groups spent more time in dark compartment (TDS) than the sham gro...

Research paper thumbnail of Ecstasy-induced caspase expression alters following ginger treatment

Basic and clinical neuroscience, 2013

Exposure to 3-4, methylenedioxymethamphetamine (MDMA) leads to cell death. Herein, we studied the... more Exposure to 3-4, methylenedioxymethamphetamine (MDMA) leads to cell death. Herein, we studied the protective effects of ginger on MDMA- induced apoptosis. 15 Sprague dawley male rats were administrated with 0, 10 mg/kg MDMA, or MDMA along with 100mg/kg ginger, IP for 7 days. Brains were removed to study the caspase 3, 8, and 9 expressions in the hippocampus by RT-PCR. Data was analyzed by SPSS 16 software using the one-way ANOVA test. MDMA treatment resulted in a significant increase in caspase 3, 8, and 9 as compared to the sham group (p < 0.001). Ginger administration however, appeared to significantly decrease the same (p < 0.001). Our findings suggest that ginger consumption may lead to the improvement of MDMA-induced neurotoxicity.

Research paper thumbnail of Transforming Growth Factor-α Improves Memory Impairment and Neurogenesis Following Ischemia Reperfusion

Cell journal, 2014

Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ven... more Stroke is most important cause of death and disability in adults. The hippocampal CA1 and sub-ventricular zone neurons are vulnerable to ischemia that can impair memory and learning functions. Although neurogenesis normally occurs in the dentate gyrus (DG) of the hippocampus and sub-ventricular zone (SVZ) following brain damage, this response is unable to compensate for severely damaged areas. This study aims to assess both neurogenesis and the neuroprotective effects of transforming growth factor-alpha (TGF-α) on the hippocampus and SVZ following ischemia-reperfusion. In this experimental study, a total of 48 male Wistar rats were divided into the following groups: surgical (n=12), phosphate buffered saline (PBS) treated vehicle shams (n=12), ischemia (n=12) and treatment (n=12) groups. Ischemia was induced by common carotid occlusion for 30 minutes followed by reperfusion, and TGF-α was then injected into the right lateral ventricle. Spatial memory was assessed using Morris water ...

Research paper thumbnail of Evaluation of Bcl-2 Family Gene Expression in Hippocampus of 3, 4-methylenedioxymethamphetamine Treated Rats

Cell journal, 2012

3,4-methylenedioxymethamphetamine (MDMA) is an illicit, recreational drug that causes cellular de... more 3,4-methylenedioxymethamphetamine (MDMA) is an illicit, recreational drug that causes cellular death and neurotoxicity. This study evaluates the effects of different doses of MDMA on the expression of apoptosis-related proteins and genes in the hippocampus of adult rats. In this expremental study,a total of 20 male Sprague Dawley rats (200-250 g ) were treated with MDMA (0, 5, 10, 20 mg/kg i.p. twice daily) for 7 days. Seven days after the last administration of MDMA, the rats were killed. Bax and Bcl-2 genes in addition to protein expressions were detected by western blot and reverse transcriptionpolymerase chain reaction (RT-PCR).Results were analyzed using one-way ANOVA and p≤0.05 was considered statistically significant. Our results showed that MDMA caused dose dependent up-regulation of Bax and down-regulation of Bcl-2 in the hippocampus. There was a significant alteration in bcl-2 and bax genes density. Changes in apoptosis-related proteins and respective genes relating to Bax...

Research paper thumbnail of Protective Effects of Borago officinalis Extract on Amyloid β-Peptide(25–35)-Induced Memory Impairment in Male Rats: A Behavioral Study

BioMed Research International, 2014

Research paper thumbnail of The protective effect of Borago Officinalis extract on amyloid β (25–35)-induced long term potentiation disruption in the dentate gyrus of male rats

Metabolic Brain Disease, 2014

Alzheimer&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disea... more Alzheimer&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease (AD) begins with impairment in synaptic functions before developing into later neurodegeneration and neural loss. In the present study we have examined the protective effects of Borago Officinalis (borage) extract on amyloid β (Aβ)--Induced long term potentiation (LTP) disruption in hippocampal dentate gyrus (DG). Wistar male rats received intrahippocampal (IHP) injection of the Aβ (25-35) and borage extract throughout gestation (100 mg/kg). LTP in perforant path- DG synapses was assessed using electrophysiology method and field excitatory post- synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured by 400 Hz tetanization. Finally, the total thiol content of hippocampus was measured using colorimetric reaction based on the Ellman&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;s method. The results showed that Aβ (25-35) significantly decreased fEPSP slope and SP amplitude comparing with the control and sham group, whereas borage extract administration increased these parameters compared to the Aβ group. Aβ induced a remarkable decrease in total thiol content of hippocampus and borage prevented the decrease of the hippocampal total sulfhydryl (SH) groups. This data suggest that Aβ (25-35) can effectively inhibit LTP in the granular cells of the DG in hippocampus, and borage supplementation reverse the synaptic plasticity in DG following Aβ treatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.

Research paper thumbnail of Attenuation of ecstasy-induced neurotoxicity by N-acetylcysteine

Metabolic Brain Disease, 2014

Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and ... more Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) can lead to spatial memory impairments and hippocampal cell death. Numerous evidence indicates that the antioxidant N-acetylcysteine (NAC) exerts protective effects in the brain. The present study evaluates the effects of NAC on MDMA-induced neurotoxicity. We intraperitoneally injected 28 adult male Sprague-Dawley rats (200-250 g) with either 0, 10 mg/kg of MDMA, or 10 mg/kg of MDMA plus 100 mg/kg of NAC. Spatial memory was assessed with a Morris Water Maze (MWM). At the end of the study, rats&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39; brains were removed to study the structure and ultrastructure of CA1, and measure Bcl-2 and Bax expressions in the hippocampus. In the MWM, NAC treatment significantly attenuated the MDMA-induced increase in distance traveled (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) and escape latency (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.001). The decreased time spent in the target quadrant in MDMA-treated animals was attenuated by NAC (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.01). NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively. These data have suggested that NAC could protect against behavioral changes and apoptosis in the hippocampus following administration of MDMA. NAC might be useful for the treatment of neurotoxicity in MDMA users.

Research paper thumbnail of Protective effects of N-acetylcysteine on 3, 4-methylenedioxymethamphetamine-induced neurotoxicity in male Sprague–Dawley rats

Metabolic Brain Disease, 2013

Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hipp... more Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hippocampal cell death. In the present study we have examined the protective effects of N-acetyl-L-cysteine (NAC) on MDMA-induced neurotoxicity. A total of 56 male Sprague Dawley rats (200-250 g) received twice daily intraperitoneal (IP) injections of 5, 10 or 20 mg/kg MDMA plus NAC (100 mg/kg). Rectal temperatures were recorded before and after daily treatment. We used a Morris water maze (MWM) to assess spatial learning and memory. At the end of the study rats&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39; brains were removed, cells were counted and the level of Bcl-2, Bax and caspase-3 expression in the hippocampi were measured. NAC pretreatment significantly reduced MDMA-induced hyperthermia. In the MWM, NAC significantly attenuated the MDMA-induced increase in distance traveled; however the observed increase in escape latency was not significant. The decrease in time spent in the target quadrant in MDMA animals was significantly attenuated (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.001, all groups). NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2. This data suggested a possible benefit of NAC in the treatment of neurotoxicity among those who use MDMA.

Research paper thumbnail of Zingiber officinale alters 3,4-methylenedioxymethamphetamine-/INS;induced neurotoxicity in rat brain

Journal of the Neurological Sciences, 2013