ArticleBMC neuroscience2017
Astaxanthin protects astrocytes against trauma-induced apoptosis through inhibition of NKCC1 expression via the NF-κB signaling pathway.
Article in BMC neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Functional Recovery Promotion After Spinal Cord Injury With Astaxanthin Treatment in Preclinical Studies: A Systematic Review and Meta-Analysis.Neurology research international · 2025Review
- Evaluation of the Choroid Plexus Epithelium Inflammation TLR4/NF-κB/NKCC1 Signal Pathway Activation in the Development of Hydrocephalus.CNS neuroscience & therapeutics · 2024Article
- Article
- Inhibiting phosphatase and actin regulator 1 expression is neuroprotective in the context of traumatic brain injury.Neural regeneration research · 2023Article
- AQP4-independent TRPV4 modulation of plasma membrane water permeability.Frontiers in cellular neuroscience · 2023Article
- Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2022Review
- TNF-α induces AQP4 overexpression in astrocytes through the NF-κB pathway causing cellular edema and apoptosis.Bioscience reports · 2022Article
- Astaxanthin from Crustaceans and Their Byproducts: A Bioactive Metabolite Candidate for Therapeutic Application.Marine drugs · 2022Review
- Astaxanthin as a Modulator of Nrf2, NF-κB, and Their Crosstalk: Molecular Mechanisms and Possible Clinical Applications.Molecules (Basel, Switzerland) · 2022Review
- Recent Advancements and Future Perspectives of Microalgae-Derived Pharmaceuticals.Marine drugs · 2021Review
- Astaxanthin protects spinal cord tissues from apoptosis after spinal cord injury in rats.Annals of translational medicine · 2021Article
- Adiantum capillus-veneris Linn protects female reproductive system against carbendazim toxicity in rats: immunohistochemical, histopathological, and pathophysiological studies.Environmental science and pollution research international · 2021Article
- Inhibition of the NKCC1/NF-κB Signaling Pathway Decreases Inflammation and Improves Brain Edema and Nerve Cell Apoptosis in an SBI Rat Model.Frontiers in molecular neuroscience · 2021Article
- Anti-Apoptotic Effects of Carotenoids in Neurodegeneration.Molecules (Basel, Switzerland) · 2020Review
- Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging.Marine drugs · 2020Review
- Antioxidant Therapies in Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2020Review
- Review
- Plant-Derived Antioxidants Protect the Nervous System From Aging by Inhibiting Oxidative Stress.Frontiers in aging neuroscience · 2020Review
- Transcriptional Factors and Protein Biomarkers as Target Therapeutics in Traumatic Spinal Cord and Brain Injury.Current neuropharmacology · 2020Review
- The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective.Molecules (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAstaxanthin (ATX) is a carotenoid pigment with pleiotropic pharmacological properties that is seen as a possible drug for treating cerebral ischemic injury and subarachnoid hemorrhage. Na
resultsStretch injury in cultured astrocytes lowered cell viability time-dependently, which was substantially reducing by pretreating with ATX (50 μmol/L). Stretch injury increased Bax level and cleaved caspase-3 activity, and decreased Bcl-2 level and pro-caspase 3 activity, resulting in the apoptosis of astrocytes. Additionally, stretch injury substantially raised the gene and protein expressions of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α and prompted the expression and nuclear translocation of NF-κB. Pretreatment with ATX remarkably prevented the trauma-induced initiation of NF-κB, expressions of pro-inflammatory cytokines, and cell apoptosis. Moreover, stretch injury markedly elevated the gene and protein expression of NKCC1, which was partly blocked by co-treatment with ATX (50 µmol/L) or an NF-κB inhibitor (PDTC, 10 µmol/L). Cleaved caspase-3 activity was partially reduced by PDTC (10 µmol/L) or an NKCC1 inhibitor (bumetanide, 50 µmol/L).
conclusionsATX attenuates apoptosis after stretch injury in cultured astrocytes by inhibiting NKCC1 expression, and it acts by reducing the expression of NF-κB-mediated pro-inflammatory factors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.