ArticleAnnals of clinical and translational neurology2020
Neuroprotective effects of FK866 against traumatic brain injury: Involvement of p38/ERK pathway.
Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Targeting the mitochondrial thermogenesis pathway for neuroprotection in neonatal hypoxic-ischemic encephalopathy by curcumin.Acta pharmacologica Sinica · 2026Article
- Intracellular NADJournal of cellular and molecular medicine · 2026Article
- Aerobic exercise combined with FK866 ameliorates Alzheimer's disease-like pathology in APP/PS1 mice with NAMPT abnormality.Frontiers in immunology · 2026Article
- Network Pharmacology Combined with an Experimental Validation Study to Reveal the Effect and Mechanism ofFoods (Basel, Switzerland) · 2023Article
- Protective effects of NAMPT or MAPK inhibitors and NaR on Wallerian degeneration of mammalian axons.Neurobiology of disease · 2022Article
- Adipokines as Immune Cell Modulators in Multiple Sclerosis.International journal of molecular sciences · 2021Review
- Hydrogen gas post-conditioning alleviates cognitive dysfunction and anxiety-like behavior in a rat model of subarachnoid hemorrhage.Experimental and therapeutic medicine · 2021Article
- Lipopolysaccharide-Induced Microglial Neuroinflammation: Attenuation by FK866.Neurochemical research · 2021Article
- Cerebrospinal Fluid MicroRNA Changes in Cognitively Normal Veterans With a History of Deployment-Associated Mild Traumatic Brain Injury.Frontiers in neuroscience · 2021Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveFK866 is an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which exhibits neuroprotective effects in ischemic brain injury. However, in traumatic brain injury (TBI), the role and mechanism of FK866 remain unclear. The present research was aimed to investigate whether FK866 could attenuate TBI and clarified the underlying mechanisms.
methodsA controlled cortical impact model was established, and FK866 at a dose of 5 mg/kg was administered intraperitoneally at 1 h and 6 h, then twice per day post-TBI until sacrifice. Brain water content, Evans blue dye extravasation, modified neurological severity scores (mNSS), Morris water maze test, enzyme-linked immunosorbent assay (ELISA), immunofluorescence staining, and western blot were performed.
resultsThe results demonstrated that FK866 significantly mitigated the brain edema, blood-brain barrier (BBB) disruption, and ameliorated the neurological function post-TBI. Moreover, FK866 decreased the number of Iba-1-positive cells, GFAP-positive astrocytes, and AQP4-positive cells. FK866 reduced the protein levels of proinflammatory cytokines and inhibited NF-κB from translocation to the nucleus. FK866 upregulated the expression of Bcl-2, diminished the expression of Bax and caspase 3, and the number of apoptotic cells. Moreover, p38 MAPK and ERK activation were significantly inhibited by FK866.
interpretationFK866 attenuated TBI-induced neuroinflammation and apoptosis, at least in part, through p38/ERK MAPKs signaling pathway.
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