ArticleJournal of neural transmission (Vienna, Austria : 1996)2008
Targeting IKK2 by pharmacological inhibitor AS602868 prevents excitotoxic injury to neurons and oligodendrocytes.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- NF-κB Pathway and Its Inhibitors: A Promising Frontier in the Management of Alzheimer's Disease.Biomedicines · 2023Review
- The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Amelioration of LPS-induced inflammation response in microglia by AMPK activation.BioMed research international · 2014Article
- Sustained, neuron-specific IKK/NF-κB activation generates a selective neuroinflammatory response promoting local neurodegeneration with aging.Molecular neurodegeneration · 2013Article
- TAp63 is a transcriptional target of NF-kappaB.Journal of cellular biochemistry · 2010Article
- Unique aspects of transcriptional regulation in neurons--nuances in NFkappaB and Sp1-related factors.Journal of neuroinflammation · 2009Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Among the diverse mechanisms involved in the pathophysiology of post-ischemic and post-traumatic injuries, excitotoxicity and nuclear factor-kappaB (NF-kappaB) activation through induction of IkappaB kinase (IKK) complex have a primary role. We investigated the effects of the selective inhibitor of the IKK2 subunit, the anilinopyrimidine derivative AS602868, on excitotoxic injury produced in rat organotypic hippocampal slices and cerebellar primary neurons. Brief exposure to N-methyl-D-aspartate (NMDA) induces astrocyte reactivity, neuron cell death and oligodendrocyte degeneration in hippocampal slices. Application of AS602868 elicited a long-lasting protection of both neurons and oligodendrocytes. Maximal effect was observed with prolonged application of the compound after NMDA exposure. Neuroprotection was also evident in primary cultures of cerebellar granule cells starting from 20 nM concentration. AS602868-elicited neuroprotection correlated with inhibition of NF-kappaB activity. Our results suggest that AS602868 may prove to be a valuable approach in treating neurodegeneration and demyelination associated with cerebral trauma and ischemia.
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