Protective effect of edaravone against manganese-induced toxicity in cultured rat astrocytes

Evren, Vedat; Apaydin, Melda; Khalilnezhad, Asghar; Erbaş, Oytun; Taşkıran, Dilek

doi:10.1016/j.etap.2015.08.010

Cited by 16 publications

(6 citation statements)

References 24 publications

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“…After various treatments, astrocytes were stained with Hoechst 33342 kit (St. Louis, MO, USA) and counted blindly as described previously [ 31 ]. Briefly, astrocytes on coverslips were rinsed with PBS and fixed with 4% paraformaldehyde for 30 min.…”

Section: Methodsmentioning

confidence: 99%

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2-arachidonyl glycerol modulates astrocytic glutamine synthetase via p38 and ERK1/2 pathways

Wang

Zhang

Geng

et al. 2018

J Neuroinflammation

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BackgroundThe glutamine synthetase (GS), an astrocyte-specific enzyme, is involved in lipopolysaccharide (LPS)-induced inflammation which activates the mitogen-activated protein kinase (MAPK) signaling. Endocannabinoid 2-arachidonyl glycerol (2-AG) has been described to serve as an endogenous mediator of analgesia and neuroprotection. However, whether 2-AG can directly influence astrocytic GS and MAPK expressions remains unknown.MethodsIn the present study, the effects of 2-AG on astrocytic GS expression, p38 and ERK1/2 expression, cell viability, and apoptosis following LPS exposure were investigated.ResultsThe results revealed that LPS exposure increased GS expression with p38 activation in the early phase and decreased GS expression with activation of ERK1/2, decrease of cell viability, and increase of apoptosis in the late phase. Inhibition of p38 reversed GS increase in the early phase while inhibition of ERK1/2 reversed GS decrease in the late phase induced by LPS exposure. 2-AG protected astrocytes from increase of apoptosis and decrease of cell viability induced by the late phase of LPS exposure. In the early phase of LPS exposure, 2-AG could suppress the increase of GS expression and activation of p38 signaling. In the late phase of LPS exposure, 2-AG could reverse the decrease of GS expression and activation of ERK1/2 induced by LPS.ConclusionThese findings suggest that 2-AG could maintain the GS expression in astrocytes to a relatively stable level through modulating MAPK signaling and protect astrocytes from LPS exposure.

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Section: Methodsmentioning

confidence: 99%

“…Cell viability was detected using 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl-tetrazolium (MTT) assay as described previously [ 31 ]. In brief, astrocytes were cultured in 96-well plates at a density of 3 × 10 4 cells/well.…”

Section: Methodsmentioning

confidence: 99%

2-arachidonyl glycerol modulates astrocytic glutamine synthetase via p38 and ERK1/2 pathways

Wang

Zhang

Geng

et al. 2018

J Neuroinflammation

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“…Another study demonstrated that a 5‐week treatment with EDA eliminated the toxic effects of rotenone on dopaminergic neurons by preventing ROS generation and mitochondrial damage . Recently, we reported the beneficial effects of EDA against Mn‐induced toxicity and apoptotic cell death in astrocytes . In the current study, we further examined whether EDA have in vivo protective effects against Mn toxicity in rats.…”

Section: Discussionmentioning

confidence: 81%

Protection by Edaravone, a Radical Scavenger, against Manganese‐Induced Neurotoxicity in Rats

Apaydin

Erbaş

Taşkıran

2016

J Biochem & Molecular Tox

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Manganese (Mn) is a required element for biological systems; however, its excessive exposure may lead to a neurological syndrome known as manganism. The aim of the present study was to assess the toxic effects of subacute exposure of Mn by measuring weight gain, motor performance, and biochemical parameters (complex I activity, lipid peroxides, and protein carbonyls) in brain mitochondria in rats. We also examined whether edaravone (EDA), a radical scavenger, exerts protective effects against Mn-induced neurotoxicity. In addition, we evaluated the accumulation of Mn in brain regions using magnetic resonance imaging. Mn-exposed rats revealed significantly impaired motor performance, weight loss, and Mn accumulation in particular brain area. Lipid peroxides and protein carbonyls were significantly increased in Mn-exposed rats, whereas complex I activity was found to be decreased. EDA treatment significantly prevented mitochondrial oxidative damage and improved motor performance. These findings suggested that EDA might serve as a clinically effective agent against Mn-induced neurotoxicity.

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“…Edaravone is a synthetic free radical scavenger whose conferring neuroprotective effects have been demonstrated in animal studies (196). In vitro, researchers have demonstrated that edaravone protects neurovascular unit components, including neurons, glial cells, and endothelial cells, from oxidative cell death (168)(169)(170). In a randomized clinical trial for acute ischemic stroke, the edaravone treatment group showed higher neurological outcomes at day 90 post-onset (171).…”

Section: Scavenge Rosmentioning

confidence: 99%

Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies

et al. 2022

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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.

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Protective effect of edaravone against manganese-induced toxicity in cultured rat astrocytes

Cited by 16 publications

References 24 publications

2-arachidonyl glycerol modulates astrocytic glutamine synthetase via p38 and ERK1/2 pathways

2-arachidonyl glycerol modulates astrocytic glutamine synthetase via p38 and ERK1/2 pathways

Protection by Edaravone, a Radical Scavenger, against Manganese‐Induced Neurotoxicity in Rats

Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies

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