Neuroprotective effects of valproic acid against hemin toxicity: Possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin–proteasomal pathway

@article{Kwon2013NeuroprotectiveEO,
  title={Neuroprotective effects of valproic acid against hemin toxicity: Possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin–proteasomal pathway},
  author={K. Kwon and Jung Nam Kim and Min Kyeong Kim and S. Y. Kim and Kyu Suk Cho and S. Jeon and H. Kim and J. Ryu and Sun-Young Han and J. Cheong and L. Ignarro and Seol-Heui Han and C. Shin},
  journal={Neurochemistry International},
  year={2013},
  volume={62},
  pages={240-250}
}
During hemorrhagic stroke induced by intracerebral hemorrhage (ICH), brain injury occurs from the deleterious actions of hemoglobin byproducts; induction of heme oxygenase-1 (HO-1) also plays a critical role in the neurotoxicity in ICH. Valproic acid (VPA), which is a commonly used drug in the treatment of epilepsy, has been reported to have neuroprotective effects against various neuronal insults including ischemic stroke. We investigated the effect of VPA on HO-1-mediated neurotoxicity in an… Expand
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Distinct role of heme oxygenase-1 in early- and late-stage intracerebral hemorrhage in 12-month-old mice
  • Z. Zhang, Y. Song, +8 authors J. Wang
  • Medicine
  • Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2017
TLDR
It is concluded that HO-1 activation mediates early brain damage after ICH but promotes neurologic function recovery in the later stage of ICH. Expand
Research Progress in Understanding the Relationship Between Heme Oxygenase-1 and Intracerebral Hemorrhage
TLDR
Recent key studies regarding the effects of HO-1 following ICH, as well as its influence on ICH prognosis are summarized to provide a theoretical basis for neuroprotective function after ICH. Expand
Temporal Expression Pattern of Hemoxygenase-1 Expression and Its Association with Vasospasm and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage
TLDR
HO-1 expression in CSF in patients with SAH follows a distinct temporal induction pattern and is dependent on intracranial hematoma burden, but CSF HO-1expression was unable to predict functional outcome. Expand
Protection of Momordica charantia polysaccharide against intracerebral hemorrhage-induced brain injury through JNK3 signaling pathway
TLDR
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Neuroprotection as a Potential Therapeutic Perspective in Neurodegenerative Diseases: Focus on Antiepileptic Drugs
TLDR
Although the whole of experimental data indicating that neuroprotection can be achieved is remarkable and encouraging, no firm data have been produced in humans so far and, at the present time, neuroprotection still remains a challenge for the future. Expand
Hepcidin Protects Neuron from Hemin-Mediated Injury by Reducing Iron
TLDR
It is concluded that hepcidin protects neuron from hemin-mediated injury by reducing iron via inhibition of expression of iron transport proteins. Expand
Heme Induces BECN1/ATG5-Mediated Autophagic Cell Death via ER Stress in Neurons
TLDR
The findings suggest that heme potentiates neuronal autophagy via ER stress, which in turn induces cell death via the BECN1/ATG5 pathway, which might be a promising therapeutic strategy for ICH. Expand
Oxidative Stress in Intracerebral Hemorrhage: Sources, Mechanisms, and Therapeutic Targets
TLDR
This review will discuss the sources, possible molecular mechanisms, and potential therapeutic targets of OS in ICH, the most common cause of brain injury after ICH. Expand
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