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Paraquat induces oxidative stress, mitochondrial dysfunction, and dopaminergic neuron loss, mimicking key PD features. Bioinformatic analyses, including Reactome pathway mapping and molecular docking, confirmed a high-affinity interaction between NPS and its receptor NPSR1, activating GPCR-associated signaling. NPS treatment restored intracellular dopamine and ATP levels and increased tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT) expression. Cell viability was assessed using the MTT assay, while dopamine levels were measured via LC\u2013MS\/MS. p-ERK1\/2, total ERK1\/2, and Nrf2 were quantified by ELISA and western blot. Oxidative stress markers, including TBARS, MAO-A, MAO-B, and COMT, were analyzed by ELISA. Gene expression of Bax, Bcl-2, Caspase-3, Caspase-8, DAT, and VMAT was evaluated by qRT-PCR. TH, c-Fos, and NPSR1 were visualized using immunofluorescence. NPS significantly improved cell viability and restored ATP levels compromised by paraquat exposure. It also reduced TBARS, MAO-B, and COMT levels, reversed paraquat-induced ERK1\/2 phosphorylation, and restored Nrf2 and MAO-A expression. Additionally, NPS upregulated the anti-apoptotic marker Bcl-2. Most of these protective effects were abolished in the presence of the NPSR antagonist ML154, indicating a receptor-mediated mechanism of action. In conclusion, NPS was found to attenuate oxidative stress, support mitochondrial and dopaminergic function, and influence apoptosis-related signaling in our cellular model. These findings suggest that targeting the NPS\/NPSR1 system may hold therapeutic potential in neurodegenerative diseases such as PD, warranting further in vivo validation.<\/jats:p>\n                  <jats:p>\n                    <jats:bold>Graphical Abstract<\/jats:bold>\n                  <\/jats:p>","DOI":"10.1007\/s12035-025-05401-7","type":"journal-article","created":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T06:26:20Z","timestamp":1770013580000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Neuropeptide S Protects Dopaminergic Neurons in a Paraquat-Induced Parkinson\u2019s Model Using SH-SY5Y Cells"],"prefix":"10.1007","volume":"63","author":[{"given":"Fatma Gonca","family":"Ko\u00e7anc\u0131","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mehmet","family":"B\u00fclb\u00fcl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u0130rem","family":"Ak\u00e7al\u0131","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dijle","family":"Kipmen-Korgun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ebral","family":"\u00c7ubuk\u00e7u","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mutay Ayd\u0131n","family":"Aslan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleyna","family":"\u00d6zt\u00fcz\u00fcn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simla Su","family":"Akkan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tug\u00e7e","family":"\u00c7eker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aysel","family":"Agar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,2]]},"reference":[{"key":"5401_CR1","doi-asserted-by":"publisher","first-page":"1294","DOI":"10.1111\/j.1460-9568.2005.04301.x","volume":"22","author":"K Ossowska","year":"2005","unstructured":"Ossowska K, Wardas J, \u015amia\u0142owska M et al (2005) A slowly developing dysfunction of dopaminergic nigrostriatal neurons induced by long-term paraquat administration in rats: an animal model of preclinical stages of Parkinson\u2019s disease? 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