NF-κB and innate immunity in ischemic stroke.
Olivier A. Harari,James K. Liao +1 more
TL;DR: The relationship between NF‐κB and ischemic stroke, its role in the neurovascular unit, and some animal models that suggest that this relationship is causal are reviewed.
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Abstract: Acute cerebral ischemia elicits an innate immune response that leads to a cascade of events that culminates in necrotic death of neurons and injury to their supportive structures in the neurovascular unit. Indeed, clinical studies have shown a close relationship between elevated levels of inflammatory markers and the risk for ischemic stroke. However, the signaling pathways that link these events are not well understood. A central regulator of inflammatory response is the transcription factor, nuclear factor-kappa B (NF-κB). The activation of NF-κB is required for the transcriptional induction of many proinflammatory mediators involved in innate immunity, such as cellular adhesion molecules, cytokines, and growth factors. Therefore, factors that modulate the activity of NF-κB could potentially regulate inflammatory processes in ischemic stroke. Here, we review the relationship between NF-κB and ischemic stroke, its role in the neurovascular unit, and discuss some animal models that suggest that this relationship is causal.
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NLRP3 deficiency ameliorates neurovascular damage in experimental ischemic stroke
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References
Selective Inhibition of Nuclear Factor-κB Activation After Hypoxia/Ischemia in Neonatal Rats Is Not Neuroprotective
Evelyn van den Tweel,Annemieke Kavelaars,Maria Stella Lombardi,Floris Groenendaal,Michael May,Cobi Jacoba Johanna Heijnen,Frank van Bel +6 more
TL;DR: Analysis of long-term cerebral damage revealed that inhibition of NFκB activation by administration of NBD peptide at 0, 6, and 12 h after HI resulted in an increment of neuronal damage.
Atorvastatin protects rat brains against permanent focal ischemia and downregulates HMGB1, HMGB1 receptors (RAGE and TLR4), NF-κB expression
TL;DR: It is found that atorvastatin dramatically improved neurological deficits, reduced brain water contents and infarct sizes at 24h after stroke, and the over-expression of HMGB1, RAGE, TLR4 and NF-kappaB induced by ischemia was significantly attenuated by atorVastatin.
Neuronal activation of NF-κB contributes to cell death in cerebral ischemia
Wen Zhang,Ioana Potrovita,Victoria Tarabin,Oliver Herrmann,Verena Beer,Falk Weih,Armin Schneider,Markus Schwaninger +7 more
TL;DR: The data show that NF-κB is activated in neurons and astrocytes during cerebral ischemia and that NF -κB activation in neurons contributes to the ischemic damage.