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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.