Glutamate Receptor-Mediated Neuronal Death in the Ischemic Brain

1997 ◽  
pp. 1-13 ◽  
Author(s):  
D.W. Choi ◽  
D. Lobner ◽  
L.L. Dugan
Keyword(s):  
Glutamate Receptor ◽  
Neuronal Death ◽  
Ischemic Brain

Abstract TP97: Korean Red Ginseng Ameliorates Cerebral Hypoxic-Ischemic Damage Through the Activation of the Nrf2 Pathway by Preferentially Altering Reactive Astrogliosis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Lei Liu ◽  
Mary K. Vollmer ◽  
Morgan W. Carson ◽  
Todd J. Sahagian ◽  
Hocheol Kim ◽  
...  
Keyword(s):  
Brain Damage ◽  
Neuronal Death ◽  
Ischemic Damage ◽  
Protective Effects ◽  
Red Ginseng ◽  
Korean Red Ginseng ◽  
Neuroprotective Effects ◽  
Edema Formation ◽  
Ischemic Brain ◽  
Nrf2 Pathway

Introduction: Endogenous defense mechanisms by which the brain protects itself against noxious stimuli and recovers from ischemic damage are key targets of stroke research that may ultimately facilitate functional recovery. Multiple evidences indicate that the transcriptional factor Nrf2 plays a vital role in cellular defense against oxidative stress and inflammation, and consequently, targeting Nrf2 has emerged as a promising therapeutic strategy for disease prevention. Korean Red Ginseng (Ginseng), one of the most widely used herbal medicines in the world, has been suggested as one of the most potent Nrf2 activators, thereby making it efficacious against various acute neurological disorders, including stroke. Hypothesis: To evaluate whether Ginseng could exert protective effects against hypoxic-ischemic brain damage and whether Nrf2 activation is pivotal to the various neuroprotective effects of Ginseng. Methods: C57BL/6 WT and Nrf2 knockout mice (10-18 weeks old, n=12-16) were orally administered Ginseng (100mg/kg/d) or vehicle 7d prior to cerebral hypoxic-ischemic damage. At 6 and 24h after stroke, mice were neurologically scored. Brain lesion size and edema formation were measured at 24h. Using immunostaining, we examined which cells appeared to be most preferentially activated in a spatiotemporal pattern by this Nrf2 pathway, in particular, in the early stage of ischemic injury. Based on the results, we are further evaluating the efficacy of inducing the Nrf2 pathway and assess the extended neuroprotective effects of Ginseng at 7d after stroke. Results: Ginseng treatment significantly reduced cerebral infarct size, neuronal death, edema formation and the resultant functional neurological deficits at 24h after stroke (P<0.001); whereas, Nrf2 ablation remarkably attenuated all benefits. Notably, the above protective effects of Ginseng were significantly attenuated in Nrf2 knockouts (P<0.05). In addition, Ginseng treated mice also exhibited reduced neuronal death and delayed severe reactive astrogliosis at 6 and 12h (P<0.05). Conclusion: Our findings indicate a neuroprotective effect of Ginseng against hypoxic-ischemic brain damage, and that Nrf2-dependent cytoprotective responses appear to be more prominent in astrocytes.

Post-ischemic brain damage: the endocannabinoid system in the mechanisms of neuronal death

FEBS Journal ◽  
2008 ◽  
Vol 276 (1) ◽  
pp. 2-12 ◽  
Author(s):  
Domenico E. Pellegrini-Giampietro ◽  
Guido Mannaioni ◽  
Giacinto Bagetta
Keyword(s):  
Brain Damage ◽  
Neuronal Death ◽  
Endocannabinoid System ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

RNPS1 inhibition aggravates ischemic brain injury and promotes neuronal death

2020 ◽  
Vol 523 (1) ◽  
pp. 39-45
Author(s):  
Zhi Zhang ◽  
Mengdi Guo ◽  
Ying Liu ◽  
Pinyi Liu ◽  
Xiang Cao ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuronal Death ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

scholarly journals Reduction of Ischemic Brain Damage by Nitrous Oxide and Xenon

2003 ◽  
Vol 23 (10) ◽  
pp. 1168-1173 ◽  
Author(s):  
Helene N David ◽  
Frederic Leveille ◽  
Laurent Chazalviel ◽  
Eric T MacKenzie ◽  
Alain Buisson ◽  
...  
Keyword(s):  
Nitrous Oxide ◽  
Brain Damage ◽  
Neuronal Death ◽  
Cortical Cell ◽  
Critical Event ◽  
Neuroprotective Agents ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Neurotoxic Effects

Neuronal death after ischemia-induced brain damage depends largely upon the activation of the N-methyl-D-aspartate (NMDA) excitatory glutamate receptor that is a target for many putative neuroprotective agents. Whereas the NMDA receptors mediate ischemic brain damage, blocking them is deleterious in humans. Here, the authors investigated whether nitrous oxide or xenon, which are gaseous anesthetics with a remarkably safe clinical profile that have been recently demonstrated as effective inhibitors of the NMDA receptor, may reduce the following: (1) ischemia-induced brain damage in vivo, when given after occlusion of the middle cerebral artery (MCAO), a condition needed to make these potentially neuroprotective agents therapeutically valuable; or (2) NMDA-induced Ca2+ influx in cortical cell cultures, a major critical event involved in excitotoxic neuronal death. The authors have shown that both nitrous oxide at 75 vol% and xenon at 50 vol% reduce ischemic neuronal death in the cortex by 70% and further decrease NMDA-induced Ca2+ influx by 30%. In addition, xenon at 50%, but not nitrous oxide at 75 vol%, further decreases ischemic brain damage in the striatum (a subcortical structure that is known to be resistant to neuroprotective interventions). However, at a higher concentration (75 vol%), xenon exhibits potentially neurotoxic effects. The mechanisms of the neuroprotective and potentially neurotoxic effects of nitrous oxide and xenon, as well as the possible therapeutic implications in humans, are discussed.

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