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 Background & objectives: Stroke remains one of main causes of death and disability in human. Animal models of the brain ischemia provide an important roles for studying of the pathophysiological mechanisms and evaluating of the efficacy of neuroprotective agents. The aim of this study is introducing a new model of the focal cerebral ischemia with increased success and low mortality rate.

 Methods: Fifteen six male mice were anesthetized with isofolorane and mixture of O2/N2O divided in four groups. Focal cerebral ischemia was induced by intraluminal filament method. A silicon coated nylon filament was used for middle cerebral artery occlusion. Regional cerebral blood flow was monitored by laser Doppler flowmetery for leading of filament in vascular pathway. In the 24 hours following ischemia (60minutes), animals were assessed for neurological outcome, infarct volume and brain edema induction. A new and reformed neurological test was used for evaluation of neurological deficits. 10 µm coronal sections were collected from 12 levels of the brain and stained, digitized and quantified by using an image analysis system. Ischemic brain edema was investigated by brain water content detection.

 Results: When sham operated mice had no motor deficit and infarction, induction of ischemia in ischemic group, seriously caused impairment of motor functions (neurological deficit score 3.36±0.25). Mean total infarct volume of left (ischemic) hemisphere was 85.2±4.9 mm³ and 47 percent of infarction occurred in subcortical regions of the brain. Induction of focal cerebral ischemia in the left (ischemic) hemisphere of the brain significantly increased water content (83.1±0.29 percent) compared to both hemispheres of sham group and right hemisphere of the same group. Success rate of ischemia induction was 97.6 percent and mortality rate was 4.21 percent.

 Conclusion: These findings indicate. This present model can be used for brain ischemia studies with high success rate, low mortality rate and narrow variety of the size and location of infarct volume. This model provides controlled and standard conditions to study ischemic brain injury and edema formation and introduce new therapeutic strategies.

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 Background & objectives: Ischemic brain edema is one of the most important complications of cerebral infarction. Edema aggravates the primary ischemic injury to the brain. It was demonstrated that the renin-angiotensin system (RAS) and its active peptide angiotensin II involved in ischemic brain injury. But role of RAS in the formation of ischemic edema is not clear. The present study was conducted to investigate the effects of the RAS inhibition by enalapril on edema formation and blood-brain barrier (BBB) disruption.

 Methods: In this research frothy Sprague Dawley male rat in six groups were studied. Animals were anesthetized with chloral hydrate (400mg/kg, IP). Transient focal cerebral ischemia was induced by occlusion of right middle cerebral artery using intraluminal filament method. Three groups of animals as sham, ischemic and enalapril receiving (0.03mg/kg) groups were studied for assessment of neurological outcome and brain edema formation. 24 hours following ischemia (60minutes), animals were assessed for neurological deficits. Ischemic brain edema was investigated by brain water content detection. Another three groups of animals at the same conditions were studied to evaluate the possible disruption of BBB by Evans blue extravasation technique.

 Results: When sham operated rats had no motor deficit, induction of ischemia in ischemic group, seriously caused impairment of motor functions and neurological deficit score(NDS) of ischemic group was 2.67±0.42. Pretreatment with enalapril (0.03mg/kg) significantly reduced NDS and improved motor dysfunctions (1.5±0.34, P<0.05). Induction of ischemia seriously caused edema formation in right (ischemic) hemisphere of the brain in ischemic group (4.1±0.4 percent). Pretreatment with enalapril (0.03mg/kg) significantly decreased edema compared to ischemic group (1.89±0.23 percent). Extravasation of Evans blue in right side of the brain in ischemic group (12.48±1.94 μg/g) was significantly more than sham group. Pretreatment with enalapril (0.03mg/kg) had protective effects on BBB function and decreased Evans blue extravasation by 44.5 percent (6.92±1.46 μg/g).

 Conclusion: RAS�inhibition by enalapril reduces ischemic brain edema formation by protecting the integrity of BBB and reducing its permeability following focal cerebral ischemia in rat. Pre-ischemic inhibition of RAS activity may reduce ischemic brain injury by ameliorating edema formation.

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  Background & objectives: Ischemic stroke is the third leading cause of death and disability in most of the human societies. There is no effective treatment due to complexity of the pathophysiological mechanisms. Today, more researches are designed to introduce involving factors and new treatment strategies in brain ischemia. The objective of this study is to introduce an experimental model of the focal cerebral ischemia in rat with increased success rate and low mortality rate.

  Methods: In this research 32 male rats (Sprague-Dawley) were studied as in four experimental groups. Animals were anesthetized with chloral hydrate (400mg/kg, ip). Focal cerebral ischemia was induced by intraluminal filament method. A silicon coated nylon filament was used for middle cerebral artery occlusion. Regional cerebral blood flow was monitored by laser Doppler flowmetery to guide the insertion of the filament into the vascular pathway. 24 hours after ischemia (90minutes), animals were assessed for neurological outcome, infarct volume and brain edema formation. A new and reformed neurological test was used for evaluation of neurological deficits. 2 - millimeter coronal sections were collected from 6 levels of the brain and stained, digitized and quantified by using an image analysis system. Ischemic brain edema formation was investigated by brain water content detection.

  Results: Induction of ischemia in ischemic group, seriously caused impairment of motor functions (neurological deficit score 4±0.5) While sham operated rats had no motor deficit and infarction. Mean total infarct volume of left (ischemic) hemisphere was 402±43 mm³ and 62.7 percent of infarction occurred in cortical regions of the brain. Induction of focal cerebral ischemia in the left (ischemic) hemisphere of the brain significantly increased water content (84±0.23 percent) compared to both hemispheres of sham group and right hemisphere of the same group. Success rate of ischemia induction was 100 percent and there was no mortality due to technical problems.

  Conclusion: Our findings indicate that continuous recording of regional cerebral blood flow using laser Doppler flowmeter had significant role in increasing success rate and lowering mortality rate in the present model of ischemic rat. This experimental model with high success rate and low limitation can be used for brain ischemia studies and evaluating new therapeutic strategies.

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  Background & objectives: Brain ischemia leads to irreversible functional and structural damage in various regions of the brain, especially in the hippocampus. There is an evidence indicating the physical exercise has neuroprotective effects and may decrease the cerebral ischemia/ reperfusion injury in rats. The purpose of this study was the study of the effect of exercise preconditioning on memory deficits and neuronal cell death in CA3 pyramidal cells of the rat hippocampus following transient global ischemia.

  Methods: 21 male rats weighing 260-300g were randomly selected and allocated into three groups (sham, ischemia and exercise+ischemia). The rats in exercise group were trained to run on a treadmill 5 days a week for 4 weeks. Ischemia induced by occlusion both common carotid arteries (CCA) for 20 minutes. The passive avoidance memory test using a Shuttle box used to assess the impairment of memory. The amount of cell death was measured using cresyl violet staining method.

  Results: The results showed that cerebral ischemia is associated with memory impairment, and physical activity before ischemia improves ischemia-induced memory impairments significantly (p<0.05). In addition, ischemia leads to cell death in hippocampal CA3 area neurons and exercise also reduces ischemia-induced cell death significantly (p<0.05).

  Conclusion: This study showed that exercise, when is used as a preconditioning stimulant , has a neuroprotective effects against brain ischemia.

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Background & objectives: One of the most important causes of acute kidney injury is ischemia-reperfusion (IR). Some studies have shown that adenosine A1 receptor inhibition have protective effects against Ischemia–reperfusion induced renal injuries, while other studies have demonstrated the opposite. The aim of the present study was to review the methodology of these studies to reach a final conclusion about the effects of adenosine A1 receptor on ischemia-reperfusion-induced renal injuries.
Methods: Data base motors including Scopus, PubMed, Google Scholar, Science Direct and Embase were searched. The terms and keywords used included ischemia-reperfusion, acute kidney injury, acute renal failure, A1 adenosine receptor and their combination.
Results: Increased adenosine levels following renal Ischemia-reperfusion cause vasoconstriction in afferent arteriole and vasodilatation in efferent arteriole through A1 adenosine receptor activation, which in turn reduces glomerular filtration rate (GFR). Inhibition of A1 adenosine receptor leads to short-term correction of renal functional parameters following renal Ischemia-reperfusion, by increasing renal blood flow and thus improving GFR. But this increase in GFR exacerbates kidney damages through the kidneys workload enhancement, which will show up in the next few hours.
Conclusions: Although selective inhibition of A1 adenosine receptor in the short term improves renal function parameters, but exacerbates renal damages in the following hours. Therefore, adenosine A1 receptor stimulation has protective effects against IR-induced kidney injury.

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Background& objectives: Renal ischemia-reperfusion (IR) damage occurs during renal transplantation in end-stage renal disease (ESRD) patients which activate immune responses. Inflammatory responses by increased levels of cytokines can lead to acute kidney injury (AKI) that contributes to the loss of renal grafts and graft dysfunction. The purpose of this study was to review the therapeutic effects of nanoparticles in AKI.
Methods: A comprehensive search strategy was identified relevant studies on AKI models, using the Scopus, PubMed and Google Scholar databases, from 2000 until 2020. The search strategy included keywords like ischemia-reperfusion and nanoparticles.
Results: Oxygen free radicals are produced during the reperfusion phase, which cause lipid peroxidation and promote tissue damage. Oxidative damage to DNA and proteins and lipid membrane peroxidation can cause cell death and apoptosis. Some strategies to reduce the tissue damage caused by ischemia-reperfusion are nanoscale materials. Antioxidant nanoparticles reduce oxidative stress in tissues. Also, they have flexibility in the delivery of therapeutic agents and drugs to the ischemic cells, and imaging of the ischemic regions at the molecular or cellular level.
Conclusion: This potential of antioxidant and anti-inflammatory nanoparticles in the diagnosis and treatment of renal ischemic regions is an innovation in the development of new therapies and a unique achievement in recent medical advances.