CCL11 enhances excitotoxic neuronal death by producing reactive oxygen species in microglia

Glia ◽  
2015 ◽  
Vol 63 (12) ◽  
pp. 2274-2284 ◽  
Author(s):  
Bijay Parajuli ◽  
Hiroshi Horiuchi ◽  
Tetsuya Mizuno ◽  
Hideyuki Takeuchi ◽  
Akio Suzumura
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Excitotoxic Neuronal Death

S2-2 Neuronal death induced by reactive oxygen species

1996 ◽  
Vol 25 ◽  
pp. S5
Author(s):  
Takumi Satoh ◽  
Yasushi Enokido ◽  
Hiroshi Hatanaka
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Death ◽  
Reactive Oxygen ◽  
Oxygen Species

Protective effects of sodium para-amino salicylate on manganese-induced neuronal death: the involvement of reactive oxygen species

2009 ◽  
Vol 61 (11) ◽  
pp. 1563-1569
Author(s):  
Hyonok Yoon ◽  
Do-Sung Kim ◽  
Geum-Hwa Lee ◽  
Ji Ye Kim ◽  
Diana H. Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protective Effects

scholarly journals Protection of Hypoglycemia-Induced Neuronal Death by β-Hydroxybutyrate Involves the Preservation of Energy Levels and Decreased Production of Reactive Oxygen Species

2015 ◽  
Vol 35 (5) ◽  
pp. 851-860 ◽  
Author(s):  
Alberto Julio-Amilpas ◽  
Teresa Montiel ◽  
Eva Soto-Tinoco ◽  
Cristian Gerónimo-Olvera ◽  
Lourdes Massieu
Keyword(s):  
Reactive Oxygen Species ◽  
Protective Effect ◽  
Neuronal Death ◽  
Ketone Bodies ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Oxygen Species ◽  
Atp Production

Glucose is the main energy substrate in brain but in certain circumstances such as prolonged fasting and the suckling period alternative substrates can be used such as the ketone bodies (KB), beta-hydroxybutyrate (BHB), and acetoacetate. It has been shown that KB prevent neuronal death induced during energy limiting conditions and excitotoxicity. The protective effect of KB has been mainly attributed to the improvement of mitochondrial function. In the present study, we have investigated the protective effect of D-BHB against neuronal death induced by severe noncoma hypoglycemia in the rat in vivo and by glucose deprivation (GD) in cortical cultures. Results show that systemic administration of D-BHB reduces reactive oxygen species (ROS) production in distinct cortical areas and subregions of the hippocampus and efficiently prevents neuronal death in the cortex of hypoglycemic animals. In vitro results show that D-BHB stimulates ATP production and reduces ROS levels, while the nonphysiologic isomer of BHB, L-BHB, has no effect on energy production but reduces ROS levels. Data suggest that protection by BHB, not only results from its metabolic action but is also related to its capability to reduce ROS, rendering this KB as a suitable candidate for the treatment of ischemic and traumatic injury.

Implication of PTEN in production of reactive oxygen species and neuronal death in in vitro models of stroke and Parkinson's disease

2007 ◽  
Vol 50 (3) ◽  
pp. 507-516 ◽  
Author(s):  
Yuan Zhu ◽  
Patrick Hoell ◽  
Barbara Ahlemeyer ◽  
Ulrich Sure ◽  
Helmut Bertalanffy ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuronal Death ◽  
Reactive Oxygen ◽  
In Vitro Models ◽  
Oxygen Species

Evidence against the involvement of reactive oxygen species in the pathogenesis of neuronal death in down's syndrome and Alzheimer's Disease

Life Sciences ◽  
1996 ◽  
Vol 59 (7) ◽  
pp. 537-544 ◽  
Author(s):  
Marianne Hayn ◽  
Karl Kremser ◽  
Nicolas Singewald ◽  
Nigel Cairns ◽  
Maria Nemethova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Neuronal Death ◽  
Down's Syndrome ◽  
Reactive Oxygen ◽  
Down’S Syndrome ◽  
Oxygen Species

Protective effects of sodium para-amino salicylate on manganese-induced neuronal death: the involvement of reactive oxygen species

2009 ◽  
Vol 61 (11) ◽  
pp. 1563-1569 ◽  
Author(s):  
Hyonok Yoon ◽  
Do-Sung Kim ◽  
Geum-Hwa Lee ◽  
Ji Ye Kim ◽  
Diana H. Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Neuronal Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protective Effects

scholarly journals The Role of NADPH Oxidase in Neuronal Death and Neurogenesis after Acute Neurological Disorders

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 739
Author(s):  
Song-Hee Lee ◽  
Min-Woo Lee ◽  
Dong-Gyun Ko ◽  
Bo-Young Choi ◽  
Sang-Won Suh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Reactive Oxygen ◽  
Neuronal Injury ◽  
Oxygen Species ◽  
Comprehensive Overview

Oxidative stress is a well-known common pathological process involved in mediating acute neurological injuries, such as stroke, traumatic brain injury, epilepsy, and hypoglycemia-related neuronal injury. However, effective therapeutic measures aimed at scavenging free reactive oxygen species have shown little success in clinical trials. Recent studies have revealed that NADPH oxidase, a membrane-bound enzyme complex that catalyzes the production of a superoxide free radical, is one of the major sources of cellular reactive oxygen species in acute neurological disorders. Furthermore, several studies, including our previous ones, have shown that the inhibition of NADPH oxidase can reduce subsequent neuronal injury in neurological disease. Moreover, maintaining appropriate levels of NADPH oxidase has also been shown to be associated with proper neurogenesis after neuronal injury. This review aims to present a comprehensive overview of the role of NADPH oxidase in neuronal death and neurogenesis in multiple acute neurological disorders and to explore potential pharmacological strategies targeting the NADPH-related oxidative stress pathways.

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