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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.

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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.

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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.

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Background and Objective: Reduction in cerebral blood flow following cereblal ischemia cause the production of oxygen free radicals and finally leads to brain tissue destruction. Pyramidal cells of the CA1 region of hippocampus are highly sensitive to hypoxic condition. This study was done to determine the effect of human chorionic gonadotropin (hCG) and vitamine E on cellular density of CA1 hippocampal area, learning ability and memory, following ischemia - reperfusion injury in mice. Materials and Methods: This experimental study was done on 40 male mice in 5 groups as follow: sham control, ischemia, hCG treated, vitamine E treated and hCG + vitamine E treated groups. Single dose of vitamin E was injected intraperitonaly during the establishment of reperfusion and hCG was injected from 48h after ischemia for 5 days. Folowing the treatment period, mice brains were fixated by transcardial perfusion and stained by nissle method. The shuttle box was used to evaluate the learning memory. Results: Co-administartion of vitamine E and hCG, significantly increased the cell numbers in hippocampus compared to the ischemic group (P<0.001). Also learning and memory improved in treatment group in comparison with ischemia group (P<0.05). Conclusion: Co-administration of vitamin E and hCG improved ischemia-induced neurodegenration and memory impairment.

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Background and Objective: A brief and short duration episode of ischemia is recorded in ischemic preconditioning (IPC). This latter condition provides a status in which large region of heart is protected when prolonged ischemia occurred. Levothyroxine play a protective role in IPC induction, and simultaneously with stress oxidative. This study was conducted to determine the protective effect of levothyroxine with oxidative stress reduction mechanism in ischemic preconditioning model in rat heart.
Methods: This experimental study was performed on 30 male Wistar rats in three groups of 10, as follows. In the reperfusion ischaemia group (IR), the heart of the animal was placed in a Langendorff apparatus. In the ischemic preconditioning group (IPC), prior to major ischemia, was exposed to 4 periods of 5-minute ischemia with reperfusion. In the intraperitoneally administered group, levothyroxine at a dose of 25 microgram per 100 g of body weight, the heart was exposed to reperfusion ischemia. The area of infarct and the level of malondialdehyde in the heart tissue were measured.
Results: The volume of Infarcted region in IR and IPC groups was 26.55 and 11.11 respectively. The same index for the Levothyroxine receiver was 12.56. Based on these findings it was demonstrated that Levothyroxine injection reduced the Infarcted region significantly similar with IPC (P<0.05). The MDA Levels in IR and IPC were 1328 and 777, respectively and in Levothyroxine group it was determined as 762. The size of Infarcted region in both IPC and treated with Levothyroxine groups significantly reduced in compared to IR group (P<0.05).
Conclusion: Injection of levothyroxine with ischemic preconditioning reduced the effect of reperfusion maladaptive ischemia in rat heart.

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Background and Objective: Acute ischemic preconditioning improves exercise performance. This study was done to determine the effect of four weeks of ischemic preconditioning on vascular grow factor (VEGF), lactate metabolism and fatigue indices.
Methods: In this clinical trial study, twenty inactive young men were randomly divided experimental (n=10) and control (n=10) groups. Subjects in experimental group perceived ischemic preconditioning (consisted of four 5-minute cycles of ischemia, followed by five minutes of reperfusion) for four weeks prior training. Blood samples were taken in the rest in order to measuring of VEGF. 48 hours prior and after the last intervention session, subjects performed an anaerobic Wingate test and rating the perceived exertion immediately and blood lactate were measured before, immediately, 5, 10 and 15 min after of Wingate test.
Results: 4-week IPC treatment significantly increased VEGF in compared to control group (138.2±8.2 vs 160.1±10.3) (P<0.05). Rating of perceived exertion (6.4±0.5 vs 6±0.1) and lactate accumulation in 15 min after exercise was significantly lower in experimental group in compare to controls (4.1±0.8 vs 5.6±1.2) (P<0.05). There was no significant difference between groups for power output (745.2±131.6 vs 769.7±148.6) and fatigue index (50.58±7.2 vs 46.2±11.8).
Conclusion: Four weeks of ischemic preconditioning increase VEGF and reduce rating the perceived exertion and blood lactate after intensive exercise in inactive young men.

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Background and Objective: Stroke and cerebral ischemia are the second leading causes of death in the world. Currently, there are limited therapeutic interventions for patients with ischemia / reperfusion. This study was performed to determine the protective effect of aerobic exercise and adenosine on changes in inflammation mediators after transient ischemia of common carotid arteries in male Wistar rats.
Methods: In this experimental study, fifty male Wistar rats were randomly allocated into to 5 groups: control, cerebral ischemic control, aerobic exercise + cerebral ischemia, adenosine + cerebral ischemia and aerobic exercise + adenosine + cerebral ischemia. Ischemia was performed by blocking the common carotid artery for 45 minutes after a period of exercise and injection of adenosine. Neuronal structure was examined by Nissel tissue staining. The expression of NGF and Glutamate genes were measured in CA1 region of hippocampal tissue samples.
Results: Cell death was increased in neurons in the CA1 region of the hippocampus in the ischemia / reperfusion group, While a significant reduction in cell death in the adenosine + ischemia / reperfusion and aerobic exercise + ischemia /reperfusion groups was due to adenosine administration and aerobic exercise (P<0.05). NGF and glutamate gene expression in the adenosine + ischemia/reperfusion and adenosine + aerobic exersice + ischemia/reperfusion groups significantly increased and reduced compared to the ischemia/reperfusion control, respectively (P<0.05).
Conclusion: Co-administration of adenosine combined with aerobic exercise increase the protective effect of aerobic exercise on improving the neuronal damage after ischemic / reperfusion.