Abstract
To counteract oxidative stress and associated brain diseases, antioxidant systems rescue neuronal cells from oxidative stress by neutralizing reactive oxygen species and preserving gene regulation. It is necessary to understand the communication and interactions between brain cells, including neurons, astrocytes and microglia, to understand oxidative stress and antioxidant mechanisms. Here, the role of glia in the protection of neurons against oxidative injury and glia–neuron crosstalk to maintain antioxidant defense mechanisms and brain protection are reviewed. The first part of this review focuses on the role of glia in the morphological and physiological changes required for brain homeostasis under oxidative stress and antioxidant defense mechanisms. The second part focuses on the essential crosstalk between neurons and glia for redox balance in the brain for protection against oxidative stress.
Highlights
The brain is highly susceptible to oxidative injury because of its high rate of oxidative metabolic activity, intense production of reactive oxygen metabolites, weak antioxidant capacity, relatively high lipid content, high energy requirements, non-replicating neuronal cells, and high membrane surface to cytoplasm ratio
To develop new therapeutic interventions and diagnose the diseases that result from oxidative brain injury, it is necessary to understand the physiological functions of brain cells and the crosstalk between them
This review summarizes the current knowledge of the physiological roles and functions of astrocytes and microglia in response to oxidative stress, their interactions with neurons, and their neuroprotective capabilities
Summary
The brain is highly susceptible to oxidative injury because of its high rate of oxidative metabolic activity, intense production of reactive oxygen metabolites, weak antioxidant capacity, relatively high lipid content, high energy requirements, non-replicating neuronal cells, and high membrane surface to cytoplasm ratio. Oxidative injury induces neurodegenerative disease [1,2]. Reactive oxygen species (ROS) increase vulnerability to brain cell damage and functional decline via a redox imbalance between pro-oxidant and antioxidant agents, which induce the formation of free radicals and other reactive molecules. To develop new therapeutic interventions and diagnose the diseases that result from oxidative brain injury, it is necessary to understand the physiological functions of brain cells and the crosstalk between them. Targeting the interaction between astrocytes, microglia, and other brain cells may arrest or reverse oxidative injury, which results in neuroprotection. This review summarizes the current knowledge of the physiological roles and functions of astrocytes and microglia in response to oxidative stress, their interactions with neurons, and their neuroprotective capabilities
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