ArticleCells2022
Neuroprotective Effects of Neuropeptide Y on Human Neuroblastoma SH-SY5Y Cells in Glutamate Excitotoxicity and ER Stress Conditions.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- HSV-1 Infection Differentially Modulates NPY and VIP Neuropeptide Expression in the Mouse Brain and in Human Neuronal Cells.International journal of molecular sciences · 2026Article
- Neuropeptide Y as a Neuro-Immune Checkpoint in Cancer.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- Apelin-13 confers Neuropeptide Y-mediated neuroprotection and preserves learning and allocentric memory in D-glutamic acid-induced excitotoxicity in rats.Molecular neurobiology · 2026Article
- Beneficial effects of the novel first-in-class compound DX243 on ischemic outcomes followingFrontiers in stroke · 2026Article
- Selective Receptor Modulation by Truncated Neuropeptide Y (3-36) Dissociates Vasoconstriction from Neuroprotection in Experimental Glaucoma.Molecular neurobiology · 2025Article
- OPTN protects retinal ganglion cells and ameliorates neuroinflammation in optic neuropathies.Communications biology · 2025Article
- Telomere-related gene risk model predicts prognostic and immune microenvironment alterations in prostate cancer.Scientific reports · 2025Article
- Peptidergic Systems and Neuroblastoma.International journal of molecular sciences · 2025Review
- Investigating the Therapeutic Property of Galium verum L. (GV) for MSG induced Audiogenic Epilepsy (AEs) and Neuroprotection throughCentral nervous system agents in medicinal chemistry · 2025Article
- Development of a Disease Modeling Framework for Glutamatergic Neurons Derived from Neuroblastoma Cells in 3D Microarrays.Scientific reports · 2024Article
- Neuropeptide Y receptor activation preserves inner retinal integrity through PI3K/Akt signaling in a glaucoma mouse model.PNAS nexus · 2024Article
- Glutamate and excitotoxicity in central nervous system disorders: ionotropic glutamate receptors as a target for neuroprotection.Neuroprotection (Chichester, England) · 2024Review
- Identification of the Candidate mGlu2 Allosteric Modulator THRX-195518 through In Silico Method and Evaluation of Its Neuroprotective Potential against Glutamate-Induced Neurotoxicity in SH-SY5Y Cell Line.Current issues in molecular biology · 2024Article
- Neuropeptide Y Peptide Family and Cancer: Antitumor Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Plantainoside D Reduces Depolarization-Evoked Glutamate Release from Rat Cerebral Cortical Synaptosomes.Molecules (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropeptide Y (NPY), a sympathetic neurotransmitter, is involved in various physiological functions, and its dysregulation is implicated in several neurodegenerative diseases. Glutamate excitotoxicity, endoplasmic reticulum (ER) stress, and oxidative stress are the common mechanisms associated with numerous neurodegenerative illnesses. The present study aimed to elucidate the protective effects of NPY against glutamate toxicity and tunicamycin-induced ER stress in the human neuroblastoma SH-SY5Y cell line. We exposed the SH-SY5Y cells to glutamate and tunicamycin for two different time points and analyzed the protective effects of NPY at different concentrations. The protective effects of NPY treatments were assessed by cell viability assay, and the signalling pathway changes were evaluated by biochemical techniques such as Western blotting and immunofluorescence assays. Our results showed that treatment of SH-SY5Y cells with NPY significantly increased the viability of the cells in both glutamate toxicity and ER stress conditions. NPY treatments significantly attenuated the glutamate-induced pro-apoptotic activation of ERK1/2 and JNK/BAD pathways. The protective effects of NPY were further evident against tunicamycin-induced ER stress. NPY treatments significantly suppressed the ER stress activation by downregulating BiP, phospho-eIF2α, and CHOP expression. In addition, NPY alleviated the Akt/FoxO3a pathway in acute oxidative conditions caused by glutamate and tunicamycin in SH-SY5Y cells. Our results demonstrated that NPY is neuroprotective against glutamate-induced cell toxicity and tunicamycin-induced ER stress through anti-apoptotic actions.
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