scholarly journals Ischemia-Induced Interleukin-6 as a Potential Endogenous Neuroprotective Cytokine against NMDA Receptor-Mediated Excitoxicity in the Brain

2000 ◽  
Vol 20 (6) ◽  
pp. 956-966 ◽  
Author(s):  
Carine Ali ◽  
Olivier Nicole ◽  
Fabian Docagne ◽  
Sylvain Lesne ◽  
Eric T. MacKenzie ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Interleukin 6 ◽  
Cortical Neurons ◽  
Focal Cerebral Ischemia ◽  
Calcium Ionophore ◽  
Receptor Activation ◽  
Neuronal Cultures ◽  
The Brain

In the brain, the expression of the pleiotropic cytokine interleukin-6 (IL-6) is enhanced in various chronic or acute central nervous system disorders. However, the significance of IL-6 production in such neuropathologic states remains controversial. The present study investigated the role of IL-6 after cerebral ischemia. First, the authors showed that focal cerebral ischemia in rats early up-regulated the expression of IL-6 mRNA, without affecting the transcription of its receptors (IL-6Rα: and gp130). Similarly, the striatal injection of N-methyl-d-aspartate (NMDA) in rats, a paradigm of excitotoxic injury, activated the expression of IL-6 mRNA. The involvement of glutamatergic receptor activation was further investigated by incubating cortical neurons with NMDA or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). NMDA and ionomycin (a calcium ionophore) up-regulated IL-6 mRNA, suggesting that neurons may produce IL-6 in response to the calcium influx mediated through NMDA receptors. The potential role of IL-6 during ischemic/excitotoxic insults was then studied by testing the effect of IL-6 against apoptotic or excitotoxic challenges in cortical cultures. IL-6 did not prevent serum deprivation- or staurosporine-induced apoptotic neuronal death, or AMPA/kainate-mediated excitotoxicity. However, in both mixed and pure neuronal cultures, IL-6 dose-dependently protected neurons against NMDA toxicity. This effect was blocked by a competitive inhibitor of IL-6. Overall, the results suggest that the up-regulation of IL-6 induced by cerebral ischemia could represent an endogenous neuroprotective mechanism against NMDA receptor-mediated injury.

scholarly journals Induction of Na+/Myo-Inositol Cotransporter mRNA after Focal Cerebral Ischemia: Evidence for Extensive Osmotic Stress in Remote Areas

1996 ◽  
Vol 16 (6) ◽  
pp. 1203-1210 ◽  
Author(s):  
Toshihide Yamashita ◽  
Eiji Kohmura ◽  
Atsushi Yamauchi ◽  
Shoichi Shimada ◽  
Takamichi Yuguchi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Osmotic Stress ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Organic Osmolytes ◽  
Remote Areas ◽  
Regulated Expression ◽  
Cerebral Artery Occlusion ◽  
The Brain

Myo-inositol is one of the major organic osmolytes in the brain. It is accumulated into cells through an Na+/myo-inositol cotransporter (SMIT) that is regulated by extracellular tonicity. To investigate the role of SMIT in the brain after cerebral ischemia, we examined expression of SMIT mRNA in the rat brain after middle cerebral artery occlusion, which would reflect alteration of extracellular tonicity. The expression of SMIT mRNA was markedly increased 12 h after surgery in the cortex of the affected side and lasted until the second day. Increased expression was also found in the contralateral cingulate cortex. Up-regulated expression was found predominantly in the neurons in remote areas, although nonneuronal cells adjacent to the ischemic core also expressed this mRNA. These results suggest that cerebral ischemia causes extensive osmotic stress in brain and that the neuronal cells respond to this stress by increasing SMIT expression.

scholarly journals Possible Involvement of P2X7 Receptor Activation in Microglial Neuroprotection against Focal Cerebral Ischemia in Rats

2008 ◽  
Vol 31 (6) ◽  
pp. 1121-1130 ◽  
Author(s):  
Daijiro Yanagisawa ◽  
Yoshihisa Kitamura ◽  
Kazuyuki Takata ◽  
Izumi Hide ◽  
Yoshihiro Nakata ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
P2x7 Receptor ◽  
Focal Cerebral Ischemia ◽  
Receptor Activation ◽  
P2x7 Receptor Activation

scholarly journals Zingiber officinaleMitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Jinatta Jittiwat ◽  
Terdthai Tongun ◽  
Supaporn Muchimapura ◽  
Kornkanok Ingkaninan
Keyword(s):  
Cognitive Function ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Brain Infarct ◽  
Ginger Rhizome ◽  
The Brain

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

scholarly journals The regulatory role of NF-κB in autophagy-like cell death after focal cerebral ischemia in mice

Neuroscience ◽  
2013 ◽  
Vol 244 ◽  
pp. 16-30 ◽  
Author(s):  
W.-L. Li ◽  
S.P. Yu ◽  
D. Chen ◽  
S.S. Yu ◽  
Y.-J. Jiang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Regulatory Role
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