ArticleAging2024
Orexin-A alleviates ferroptosis by activating the Nrf2/HO-1 signaling pathway in traumatic brain injury.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanism by which low-intensity focused ultrasound promotes angiogenesis and neurogenesis after traumatic brain injury in a rat model via the OXA/MAPK signaling pathway.Neural regeneration research · 2026Article
- Awakening Recovery: Enhancing Orexinergic Tone After Acute CNS Damage.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Orexin-A Mitigates Traumatic Brain Injury by Inhibiting Neuronal Ferroptosis Through Orexin Receptor 1/Nuclear Factor Erythroid 2-Related Factor 2 Signaling Pathway.Molecular neurobiology · 2025Article
- Vagus nerve stimulation: a promising strategy to combat pyroptosis and inflammation in traumatic brain injury through the OX-A/NLRP3/caspase-1/GSDMD signaling pathway.European journal of medical research · 2025Article
- Targeting Spermine Oxidase to Mitigate Traumatic Brain Injury Pathology in the Aging Brain.Antioxidants (Basel, Switzerland) · 2025Article
- [Orexin-A promotes motor function recovery of rats with spinal cord injury by regulating ionotropic glutamate receptors].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Article
- Underlying Mechanisms behind the Brain-Gut-Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic Brain Injury (TBI) has high disability and mortality rate. Oxidative stress and ferroptosis are important pathophysiological characteristics after TBI. Orexin-A (OXA) can alleviate neuronal damage in diverse neurological disorders. Nevertheless, the role and mechanism of OXA in TBI stay unknown.
objectivesThe research investigated protection influence of OXA on TBI and its potential mechanisms.
methodsMale Sprague-Dawley rats were randomly grouped into: sham, TBI, TBI + normal saline (NS) and TBI+OXA groups. TBI model was constructed in rat via modified Feeney's approach, and OXA treatment was administered following construction of TBI model.
resultsRelative to TBI+NS group, TBI+OXA group displayed greatly recovered tissue damage and neurological deficits. Additionally, OXA eased oxidative stress as well as ferroptosis in cerebral cortex of rats following TBI. Furthermore, OXA increased Nrf2 expression and regulating factors HO-1 and NQO1 in cerebral cortex of TBI rats.
conclusionsOur research found OXA may restrain ferroptosis via Nrf2/HO-1 signaling pathway activation, thereby reducing brain injury after TBI.
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