Abstract

Cerebral ischemia is one of the major diseases associated with death or disability among patients. To date, there is a lack of effective treatments, with the exception of thrombolytic therapy that can be administered during the acute phase of ischemic stroke. Cerebral ischemia can cause a variety of pathological changes, including microvascular basal membrane matrix, endothelial cell activation, and astrocyte adhesion, which may affect signal transduction between the microvessels and neurons. Therefore, researchers put forward the concept of neurovascular unit, including neurons, axons, astrocytes, microvasculature (including endothelial cells, basal membrane matrix, and pericyte), and oligodendrocytes. Numerous studies have demonstrated that exercise can produce protective effects in cerebral ischemia, and that exercise may protect the integrity of the blood-brain barrier, promote neovascularization, reduce neuronal apoptosis, and eventually lead to an improvement in neurological function after cerebral ischemia. In this review, we summarized the potential mechanisms on the effect of exercise on cerebral ischemia, by mainly focusing on the neurovascular unit, with the aim of providing a novel therapeutic strategy for future treatment of cerebral ischemia.

Highlights

  • Research on neuroprotective therapy for cerebral ischemia has been a hot topic worldwide

  • Animals and patient studies have discovered that cerebral ischemia can induce expression of Matrix metalloproteinases (MMPs), the increased activity of MMP-2 and MMP-9, which is closely related to increased cerebral microvascular permeability, blood-brain barrier (BBB) destruction, inflammatory cell invasion, and brain edema (Rosell and Lo, 2008; Kurzepa et al, 2014; Yang and Rosenberg, 2015)

  • The results demonstrate that treadmill pretraining improved the relative apparent diffusion coefficient loss after cerebral ischemia, and that T2W1 values of the ipsilateral cortex and striatum decreased within 2 days after stroke, while the brain water content and expression of AQP4 were decreased at 2 days after ischemia following pretraining

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Summary

Frontiers in Cellular Neuroscience

Cerebral ischemia is one of the major diseases associated with death or disability among patients. Cerebral ischemia can cause a variety of pathological changes, including microvascular basal membrane matrix, endothelial cell activation, and astrocyte adhesion, which may affect signal transduction between the microvessels and neurons. Researchers put forward the concept of neurovascular unit, including neurons, axons, astrocytes, microvasculature (including endothelial cells, basal membrane matrix, and pericyte), and oligodendrocytes. Numerous studies have demonstrated that exercise can produce protective effects in cerebral ischemia, and that exercise may protect the integrity of the blood-brain barrier, promote neovascularization, reduce neuronal apoptosis, and eventually lead to an improvement in neurological function after cerebral ischemia. We summarized the potential mechanisms on the effect of exercise on cerebral ischemia, by mainly focusing on the neurovascular unit, with the aim of providing a novel therapeutic strategy for future treatment of cerebral ischemia

INTRODUCTION
Cerebral Ischemia and Neuronal Injury
EXERCISE AND RESTORATION OF NEUROVASCULAR UNIT
Exercise and Neuronal Death
Exercise and Vascular Protection
Findings
CONCLUSION
Full Text
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