ArticleRedox biology2017
Neuroprotective action of N-acetyl serotonin in oxidative stress-induced apoptosis through the activation of both TrkB/CREB/BDNF pathway and Akt/Nrf2/Antioxidant enzyme in neuronal cells.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed.
- Total saponins fromJournal of ginseng research · 2026Article
- Homologous series of N-acylmelatonins: synthesis, biophysical studies, enhanced antioxidant, antimicrobial and anticancer activities.European biophysics journal : EBJ · 2026Article
- The oocyte-enriched metabolite serotonin alleviates cellular senescence and aging phenotypes in the mouse.The EMBO journal · 2026Article
- N-acetyl-L-leucine in Neurological Disorders: Mechanisms, Evidence, and Therapeutic Perspectives.Cerebellum (London, England) · 2026Review
- The Protective Effects of N-Acetylserotonin Against Cisplatin-Induced Renal Injury: A Biochemical and Histopathological Study.International journal of molecular sciences · 2026Article
- Neuroprotection by canagliflozin in a Huntington's disease model: role of HIF-1α and PI3K/AKT signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Metagenomics and metabolomics analyses of the mechanism of non-expression of natural mating behavior in captive male Malayan pangolins (Frontiers in microbiology · 2026Article
- Exploring the Connection Between BDNF/TrkB and AC/cAMP/PKA/CREB Signaling Pathways: Potential for Neuroprotection and Therapeutic Targets for Neurological Disorders.Molecular neurobiology · 2025Review
- Banxia Shumi Decoction Improves Sleep and Neural Function in Insomnia Male Rats via BDNF/TrkB/CREB-Dependent Melatonin Signaling Activation.Neurochemical research · 2025Article
- Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025Review
- Deciphering the Neuroprotective Action of Bee Venom Peptide Melittin: Insights into Mechanistic Interplay.Molecular neurobiology · 2025Review
- Association between Purpureocillium, amino acid metabolism and cognitive function in drug-naïve, first-episode schizophrenia.BMC psychiatry · 2025Article
- Unlocking Alzheimer's Disease: The Role of BDNF Signaling in Neuropathology and Treatment.Neuromolecular medicine · 2025Review
- Drofenine as a Kv2.1 inhibitor alleviated AD-like pathology in mice through AActa pharmaceutica Sinica. B · 2025Article
- Targeting 5-HT Is a Potential Therapeutic Strategy for Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Melittin - the main component of bee venom: a promising therapeutic agent for neuroprotection through keap1/Nrf2/HO-1 pathway activation.Chinese medicine · 2024Article
- Ethyl Acetate Fraction of Chestnut Honey Attenuates Scopolamine-Induced Cognitive Impairment in Mice and Glutamate-Induced Neurotoxicity in HT22 Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Harnessing BDNF Signaling to Promote Resilience in Aging.Aging and disease · 2024Review
- Targeting brain-derived neurotrophic factor in the treatment of neurodegenerative diseases: A review.Neuroprotection (Chichester, England) · 2024Review
- BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy.Journal of cellular and molecular medicine · 2024Review
36 more citing papers are in PubMed but not listed here.
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5 authors.
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Abstract
N-acetyl serotonin (NAS) as a melatonin precursor has neuroprotective actions. Nonetheless, it is not clarified how NAS protects neuronal cells against oxidative stress. Recently, we have reported that N-palmitoyl serotonins possessed properties of antioxidants and neuroprotection. Based on those, we hypothesized that NAS, a N-acyl serotonin, may have similar actions in oxidative stress-induced neuronal cells, and examined the effects of NAS based on in vitro and in vivo tests. NAS dose-dependently inhibited oxidative stress-induced cell death in HT-22 cells. Moreover, NAS suppressed glutamate-induced apoptosis by suppressing expression of AIF, Bax, calpain, cytochrome c and cleaved caspase-3, whereas it enhanced expression of Bcl-2. Additionally, NAS improved phosphorylation of tropomyosin-related kinase receptor B (TrkB) and cAMP response element-binding protein (CREB) as well as expression of brain-derived neurotrophic factor (BDNF), whereas the inclusion of each inhibitor of JNK, p38 or Akt neutralized the neuroprotective effect of NAS, but not that of ERK. Meanwhile, NAS dose-dependently reduced the level of reactive oxygen species, and enhanced the level of glutathione in glutamate-treated HT-22 cells. Moreover, NAS significantly increased expression of heme oxygenase-1, NAD(P)H quinine oxidoreductase-1 and glutamate-cysteine ligase catalytic subunit as well as nuclear translocation of NF-E2-related factor-2. Separately, NAS at 30mg/kg suppressed scopolamine-induced memory impairment and cell death in CA1 and CA3 regions in mice. In conclusion, NAS shows actions of antioxidant and anti-apoptosis by activating TrkB/CREB/BDNF pathway and expression of antioxidant enzymes in oxidative stress-induced neurotoxicity. Therefore, such effects of NAS may provide the information for the application of NAS against neurodegenerative diseases.
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