Photothrombotic Stroke as a Model of Ischemic Stroke
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REVIEW
Photothrombotic Stroke as a Model of Ischemic Stroke Anatoly B. Uzdensky 1 Received: 18 August 2017 / Revised: 14 November 2017 / Accepted: 24 November 2017 # Springer Science+Business Media, LLC, part of Springer Nature 2017
Abstract The search of effective anti-stroke neuroprotectors requires various stroke models adequate for different aspects of the ischemic processes. The photothrombotic stroke model is particularly suitable for the study of cellular and molecular mechanisms underlying neurodegeneration, neuroprotection, and neuroregeneration. It is a model of occlusion of small cerebral vessels, which provides detailed study of molecular mechanisms of ischemic cell death and useful for search of potential anti-stroke agents. Its advantages include well-defined location and size of ischemic lesion that are determined by the aiming of the laser beam at the predetermined brain region; easy impact dosing by changing light intensity and duration; low invasiveness and minimal surgical intervention without craniotomy and mechanical manipulations with blood vessel, which carry the risk of brain trauma; low animal mortality and prolonged sensorimotor impairment that provide long-term study of stroke consequences including behavior impairment and recovery; independence on genetic variations of blood pressure and vascular architecture; and high reproducibility. This review describes the current application of the photothrombotic stroke model for the study of cellular and molecular mechanisms of stroke development and ischemic penumbra formation, as well as for the search of antistroke drugs. Keywords Photothrombotic stroke . Ischemia . Penumbra . Neurodegeneration . Neuroprotection
Ischemic Stroke and Neuroprotection Problem Ischemic stroke is one of the major factors of human disability and death. It is responsible for more than 5.5 million human deaths each year worldwide [1]. Blockage of blood vessels very rapidly, for few minutes, leads to oxygen and glucose deficit, ATP depletion, generation of reactive oxygen species (ROS), oxidative stress, injury of cellular membranes, loss of ionic gradients, depolarization, excitotoxicity, edema, necrosis, and brain tissue infarct [2, 3]. In such short time, it is practically impossible not only to treat, but even to diagnose stroke. The damaging processes propagate from the infarction core to the surrounding tissue. Tissue lesion in the peri-infarct zone (or zone at risk or ischemic penumbra) develops slower, for
* Anatoly B. Uzdensky [email protected] 1
Laboratory of Molecular Neurobiology, Academy of Biology and Biotechnology, Southern Federal University, 194/1 Stachky prospect, Rostov-on-Don 344090, Russia
several hours, and this Btherapeutic window^ provides time for cell protection. The concept that ischemic penumbra (or shorter - penumbra) is potentially salvageable is the basis of numerous searches of neuroprotective medications, which can save the penumbra tissue and limit negative stroke consequences [4]. More than 1000 preclinical studies and more than 200
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