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Showing 5 results for Mehdizadeh M

Katebi M (phd), Soleimani M (phd), Farahani Pad R (medical Student), Abbasi Moghadam Ma (medical Student), Mehdizadeh M (phd), Rasouli H (phd),
Volume 12, Issue 2 (7-2010)
Abstract

Background and Objective: Until now there is no drug formulated to prevent Neuronal Loss following Brain Stroke. In this study, we compared the effects of the mitoKATP opener, diazoxide, on ultra-structural morphology changes following in cortical neurons following in-vivo ischemic injury. Materials and Methods: In this experimental study, Rats randomly allocated in eight experimental groups including sheme, positive control, 1, 5 and 25 mg/kg/body weight of Glybanclamid groups and 2, 6 and 18 mg/kg body weight of Diazoxide experimental groups, respectively. In animals in each experimental groups, only 2 hours following adminstration of Diazoxide or Glybanclamid ischemia was induced for 15 min by the 4-vessel occlusions surgery followed by 24 hours reperfusion. After tissue prosseccing, ultra-structural changes in neuronal mitochondria and nuclei were studied by electromicroscope. Results: Ultrastructural morphological changes including nuclear pyknosis, swollen mitocondria and cristae damage after iscemia were observed in control and sheme groups. These changes were severe in Glybanclamid experimental groups. Also this changes were depend on dosage of Glybanclamid. Ultrastructural changes were decreased in Diazoxide treatment group (18mg/kg body weight), but in 2 and 6mg/kg/body weight of Diazoxide groups these decreasing of Ultrastructural changes was not observed. Conclusion: This study showed that Diazoxide with dosge of 18mg/kg/body weight has neuro-protective effects on diminishing ischemia-induced structural deterioration of neuronal mitochondria and morphological apoptotic changes in nucleus.
Alipanahzade H, Soleimani M, Soleimani Asl S , Mehdizadeh M, Katebi M,
Volume 14, Issue 3 (10-2012)
Abstract

Background and Objective: Ischemia-reperfusion invoke cell death in hippocampus. This study was carried out to investigate the effect of transforming growth factor alpha (TGF-alpha) of dentyte jyrus neurons and pyramidal cells of CA1 subfiled of hippocampus following ischemia-reperfusion in rat models. Materials and Methods: This experimental study was done on 40 male Wistar rats weighing 250-300gr. Animals were divided in four groups: control (n=7), sham (n=7), ischemia (n=14) and treatment (n=14). Sham group was just under surgical stress. In ischemia and treatment groups after induction of ischemia-reperfiusion by obstruction of carotid arteries blocked for 30 minutes, reperfusion PBS (phosphate buffer salin) and subsequently TGF-alpha (50 ng) were injected stereotaxicaly in lateral ventricle, respectively. In 12 and 72 days after treatment the brains were fixated by transcardial perfusion and stained by immunohistochemestry and nissle methods. Furthermore, morris water maze was used to evaluate the learning memory. Data were analyzed using SPSS-16 and ANOVA test. Results: Injection of TGF-alpha increased the cell number in hippocampus of treatment group compared to ischemic group. TGF-alpha increased expression of neuron in dentyte jyrus of treatment group in comparison with ischemic group (P<0.05). Also spatial memory improved in treatment group in comparison with ischemia group. Conclusion: TGF-alpha improves ischemia-induced neurodegenration and memory impairment.
Zamani M (msc), Rasooli H (phd), Mehdizadeh M (phd), Nobakht M (phd), Zamani F (bsc), Soleimani M (phd),
Volume 14, Issue 4 (12-2012)
Abstract

Background and Objective: Brain ischemia is one of the most important factor of morbidity and mortality and leaving many people with mental and physical disabilities. Until now there are no appropriate medications to prevent and cure ischemic injury. This study was done to evaluate the protective effect of Adenosine A1 receptor and ascorbic acid on hippocampal neuronal density and memory disorder in ischemia reperfusion induced Rats. Materials and Methods: This experimental study was performed on the hippocampus pyramidal neurons on 56 male BALB/c mice. Animals randmly allocated into 8 groups (N=7) including: 1) intact, 2) ischemic control group, 3) ischemic, plus agonist and adenosine of A1 receptor, 4) ascorbic acid (100 mg/daily), 5) ischemic plus agonist adenosine receptor (1 mg/1 kg) one week after ischemia, 6) ischemia, ascorbic acid befor and after ischemia and A1 receptor (1 mg/1 kg) agonist after ischemia, 7) A1 receptor, antagonist (2.25 / 1 kg), one weed after ischemia, 8) Ascorbic acid (100 mg/1kg) before and after ischemia plus A1 receptor antagonist (2.25 / 1 kg) after ischemia. Ischemia induced by clamping of common carotid artery and the drugs was injected subsequently into peritoneum after reduction of inflammation of ischemic zone. The Y-maze memory test performed after completing the treatment period, afterward brains fixed and prepared for microscopic nissl staining method. The counting of pyramidal cells were performed at 53500 square micrometer of CA1. Data were analyzed using SPSS-15 and ANOVA test. Results: The Y-maze test showed extensive deficit in short-term memory in ischemic group (PA=200) but in treatment groups this deficit significantly reduced (PA=243, 248 and 265). The normal neuronal cell in ischemic group was significantly lowered (n=87) than treatment groups (n=111, 105 and 125) including ascorbic acid group (125), adenosine receptor agonist (105) and ascorbic acid plus agonist adenosine receptor (111). The number of normal neuronal cell in ischemic groups significantly is reduced compared to treatment group (P<0.05). Conclusion: This study showed that concurrent treatment of ascorbic acid and Adenosine A1 receptor agonist can significantly reduce the complications caused by brain ischemia in CA1 area of hippocampus.
Soleimani Asl S, Shekarriz N, Molavi N, Basirat A, Falahati P, Esmaeili F, Azimi Z, Sajadi F, Mehdizadeh M,
Volume 15, Issue 1 (3-2013)
Abstract

Background and Objective: Considering the role of the hippocampus in memory, this study was done to evaluate the effect of 3-4,methylenedioxymethamphetamine on CA1 hippocampal neurons in male rats. Materials and Methods: In this experimental study 18 sprague dawley male rats (200-250g) were randomly allocated into three groups as follow: control (intact), control sham and experimental groups. Sham and experimental groups were received normal salin (1 cc) and MDMA10mg/kg IP for 7 days, respectively. Following transcardial perfusion by paraformaldehid 4%, structure and ultrastructure of right CA1 hippocampus were assessed by crysel violet staining and electronic microscope. Data were analyzed using SPSS-16, ANOVA and Tukey tests. Results: There was no significant difference between control (mean=210±40.38) and sham groups (mean=199±38.7) in neuron density. Neuron number decreased significantly in experimental group (mean=98±25.4) in compare to control and sham groups (P<0.001). There was no ultrastructural abnormality in control and sham groups. Finally, ultrastructural changes with apoptosis characterized by mitochondrial cristae reduction, distribution of nuclear chromatin and loss of cytoplasmic organelles in MDMA groups. Conclusion: This study shows that MDMA administration can stimulate the cell death with apoptotic pattern in hippocampus.
Madadi Dargahi S, Eftekharzadeh M, Mahdipour A, Soleimani M, Mehdizadeh M,
Volume 17, Issue 1 (3-2015)
Abstract

Background and Objective: Stem cells are a suitable treatment method for improvement of central nervous system diseases. Neuron regeneration is occure in damaged region using stem cell transplantation. This study was done to determine the effect of bone marrow mesenchymal stem cells on memory and neuronal cells graft number in the trimethyltin chloride damaged hippocampus. Methods: In this experimental study, 28 wistar male rats were allocated into four groups including control, model, Vehicle and treatment groups. Animals were received 8 mg/kg/bw of neurotoxin trimethyltin chloride by the intraperitoneal injection for causing damaged in hippocampus. One week after intraperitoneal injection of trimethyltin chloride, stem cells was injected by stereotaxy method. Six weeks after stem cells injection, the spatial memory was assessed by Morris water maze and histological studies were done by Nissl staining and normal cells count by Olysia bio report software. Results: After bone marrow mesenchymal stem cells graft, the number of normal cells were more in the treatment group (74±15.190) in compared to the Vehicle (44.67±12.971) and Model (48.56±18.105) groups (P<0.05). Also in Morris water maze test, the treatment group (387.35±189.18), (31.30±13.67) spent shorter distance and escape latency to reach the hidden platform, but this reduced non significantly in compared to Vehicle (438.18±192.56), (40.14±14.89) and model (407.98±225.44), (37.68±17.15) groups. The model and Vehicle groups spent longer distance to reach the hidden platform in comparision with the control (275.45±165.10) group (P<0.05). Also the traveled distance in target quarter had significant increased in the treatment groups (799.80±125.91) in compared to model (588.51±136.94) and Vehicle (546.48±86.47) groups (P<0.05). Conclusion: Using the bone marrow mesenchymal stem cells leads to reduce hippocampal lesions and increase the number of pyramidal neurons and improving memory in damaged hippocampus in animal model.

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مجله دانشگاه علوم پزشکی گرگان Journal of Gorgan University of Medical Sciences
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