Abstract
Stroke is the second leading cause of global death and is characterized by high rates of mortality and disability. Oxidative stress is accompanied by other pathological processes that together lead to secondary brain damage in stroke. As the major component of the brain, glial cells play an important role in normal brain development and pathological injury processes. Multiple connections exist in the pathophysiological changes of reactive oxygen species (ROS) metabolism and glia cell activation. Astrocytes and microglia are rapidly activated after stroke, generating large amounts of ROS via mitochondrial and NADPH oxidase pathways, causing oxidative damage to the glial cells themselves and neurons. Meanwhile, ROS cause alterations in glial cell morphology and function, and mediate their role in pathological processes, such as neuroinflammation, excitotoxicity, and blood-brain barrier damage. In contrast, glial cells protect the Central Nervous System (CNS) from oxidative damage by synthesizing antioxidants and regulating the Nuclear factor E2-related factor 2 (Nrf2) pathway, among others. Although numerous previous studies have focused on the immune function of glial cells, little attention has been paid to the role of glial cells in oxidative stress. In this paper, we discuss the adverse consequences of ROS production and oxidative-antioxidant imbalance after stroke. In addition, we further describe the biological role of glial cells in oxidative stress after stroke, and we describe potential therapeutic tools based on glia cells.
Highlights
Accounting for 9% of all deaths worldwide, stroke is the second leading cause of death following ischemic heart diseases [1]
Excessive astrocyte proliferation combined with pericytes is involved in the formation of glial scar, which is thought to act as a mechanical barrier to the recovery of neurological function [72].Nuclear factor E2-related factor 2 (Nrf2) is a major antioxidant pathway in astrocytes, and researchers found that a significant reduction in the number of reactive astrocytes in the CA1 region of the hippocampus was related to activation of the Nrf2 pathway following ischemia and hypoxia [73]
We found that reactive oxygen species (ROS) and superoxide production were reduced and DNA damage was significantly alleviated in C6 astrocytes treated with melatonin [172, 173]
Summary
Accounting for 9% of all deaths worldwide, stroke is the second leading cause of death following ischemic heart diseases [1]. Hemorrhagic strokes caused by rupture of blood vessels in the cerebrum and ischemic strokes caused by occlusion of cerebral arteries constitute the two subtypes of stroke; the latter accounted for approximately 87% of all strokes [2]. The high disability rate and poor prognosis that accompany stroke have greatly increased individual and societal burden. Stroke has become a major global public health and economic concern [3]
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