Activation of Nuclear Factor-κB in the Brain after Experimental Subarachnoid Hemorrhage and Its Potential Role in Delayed Brain Injury

@article{You2013ActivationON,
  title={Activation of Nuclear Factor-$\kappa$B in the Brain after Experimental Subarachnoid Hemorrhage and Its Potential Role in Delayed Brain Injury},
  author={Wan-chun You and Chun-Xi Wang and Yun-xi Pan and Xin Zhang and Xiao-ming Zhou and Xiang-Sheng Zhang and Ji-Xin Shi and Meng-liang Zhou},
  journal={PLoS ONE},
  year={2013},
  volume={8}
}
It has been reported that inflammation is involved in brain injury after subarachnoid hemorrhage (SAH). Nuclear factor-κB (NF-κB) is a key transcriptional regulator of inflammatory genes. Here, we used pyrrolidine dithiocarbamate(PDTC), an inhibitor of NF-κB, through intracisternal injection to study the role of NF-κB in delayed brain injury after SAH. A total of 55 rabbits were randomly divided into five groups: the control group; the SAH groups including Day-3, 5, and 7 SAH groups (the… Expand
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References

SHOWING 1-10 OF 68 REFERENCES
Potential Contribution of Nuclear Factor-κB to Cerebral Vasospasm after Experimental Subarachnoid Hemorrhage in Rabbits
  • Meng-liang Zhou, Ji-Xin Shi, +5 authors H. Yin
  • Medicine
  • Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2007
TLDR
The results suggest that NF-κB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response. Expand
Activation of nuclear factor-κB in the rat brain after transient focal ischemia
TLDR
It is proposed that the highly inducible NF-κB complexes resulted from induction of p65 and activation of NF-σB in post-ischemic reactive glia, and a substantial increase in the amount of p 65 was detected due to induction in reactive astrocytes and microglia/macrophages. Expand
Global Ischemia Activates Nuclear Factor-κB in Forebrain Neurons of Rats
TLDR
Whether NF-κB was activated in vivo by global ischemia in hippocampal CA1 neurons by way of oxygen radicals, TNF-α, and IL-1β is determined by immunocytochemistry, Western blot, and gel-shift analysis. Expand
Effect of systemic LPS injection on cortical NF-κB activity and inflammatory response following traumatic brain injury in rats
TLDR
It was concluded that inflammatory response and secondary brain damage occurred in the injured brain could be highly exacerbated by endotoxemia. Expand
Neuronal Activation of NF-κB Contributes to Cell Death in Cerebral Ischemia
TLDR
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. Expand
Traumatic Spinal Cord Injury Induces Nuclear Factor-κB Activation
TLDR
First evidence for the activation of NF-κB after trauma is demonstrated, which suggests functional implications for this transcription factor in the pathogenesis of acute spinal cord injury. Expand
Drug-induced neuroprotection from global ischemia is associated with prevention of persistent but not transient activation of nuclear factor-kappaB in rats.
TLDR
The role of the transient activation of NF-kappaB observed at 24 hours may be responsible for the induction of protective factors in neurons that survive the ischemic insult, whereas the persistent activation in hippocampal neurons could be responsible of proteins that result in CA1 neuronal death. Expand
Activation of nuclear factor-kappaB in the rat brain after transient focal ischemia.
TLDR
It is proposed that the highly inducible NF- kappaB complexes resulted from induction of p65 and activation of NF-kappaB in post-ischemic reactive glia in a rat studied after transient middle cerebral artery occlusion. Expand
Estrogen attenuates nuclear factor-kappa B activation induced by transient cerebral ischemia
TLDR
This work investigated the role of NFkappaB in neuronal survival in rats that received transient middle cerebral artery (MCA) occlusion, and observed that this transient cerebral ischemia induced substantial apoptosis and inflammatory responses, including IkappaB phosphorylation, NF-kappa B activation and iNOS over-expression. Expand
Neuronal activation of NF-kappaB contributes to cell death in cerebral ischemia.
  • Wen Zhang, Ioana Potrovita, +5 authors M. Schwaninger
  • Medicine
  • Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2005
TLDR
The data show that NF-kappaB is activated in neurons and astrocytes during cerebral ischemia and thatNF-kappB activation in neurons contributes to the ischemic damage. Expand
...
1
2
3
4
5
...