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Nevertheless, almost all animal models of ischemic stroke are based on young animals.
The first evidence that EPO is able to protect tissues/organs comes from several models of ischemic injury within the central nervous system (CNS).
This is an important issue in the field of studies evaluating the impact of regenerative therapies such as stem cells in preclinical models of ischemic heart disease.
In previous studies, immunosuppressive agents such as cyclosporine A and tacrolimus have shown neuroprotection by improving neurological functions and infarct volume in models of ischemic stroke.
The aim of this study was to produce similar brain damage, using experimental models of ischemic (IS) and hemorrhagic (HS) stroke and evaluate the motor spontaneous recovery profile.
Of note, two of the most consistently down-regulated genes following ERBB2 inhibition, were EGR1 and PHLDA1, which have also been shown to be up-regulated in models of ischemic preconditioning [17].
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Meanwhile, recent research has demonstrated that T-VA exerted neuroprotective in a rat model of ischemic stroke [23].
Data of the present study indicate neuroprotective effect of MMF in the experimental model of ischemic stroke.
To evaluate the effects of allogeneic mesenchymal stem cells (MSCs) in a model of ischemic acute kidney injury (AKI).
This formulation reduced the infarct volumes by more than 50% in a mouse model of ischemic stroke.
Animal modeling of ischemic stroke serves as an indispensable tool first to investigate mechanisms of ischemic cerebral injury, secondly to develop novel antiischemic regimens.
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