Neuropeptides最新文献

{"title":"Chromogranin B: A versatile neuroendocrine protein regulating physiological and metabolic functions","authors":"Chandramouli Mukherjee,&nbsp;Palki Chauksey,&nbsp;Aamna Jain,&nbsp;Bhavani S. Sahu","doi":"10.1016/j.npep.2025.102548","DOIUrl":"10.1016/j.npep.2025.102548","url":null,"abstract":"<div><div>Chromogranin B (CHGB) is a key member of the granin family of acidic proteins, predominantly localized in the secretory granules of professional secretory cells, such as neurons and neuroendocrine cells. It plays a crucial role in the regulated secretory pathway, influencing hormone storage, processing, and release. CHGB's role extends from cellular processes to systemic physiology, encompassing vesicular trafficking, calcium homeostasis, and immune regulation. CHGB dysfunction is linked to pathological conditions such as neurodegenerative diseases, cardiovascular disorders, and metabolic disorders. This review examines the multifaceted functions of CHGB at both the cellular and organismal levels, highlighting its role in maintaining cellular homeostasis and its potential link to metabolic dysfunction and related pathophysiology.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102548"},"PeriodicalIF":2.7,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of neurokinin B promotes functional recovery in traumatic brain injury by increasing M2 microglia","authors":"Fangjie Luo ,&nbsp;Xiaoyun Li ,&nbsp;Zhanpeng Zhu","doi":"10.1016/j.npep.2025.102549","DOIUrl":"10.1016/j.npep.2025.102549","url":null,"abstract":"<div><div>Microglial polarization into pro-inflammatory M1 and anti-inflammatory M2 phenotypes is critical for regulating neuroinflammation and tissue repair following traumatic brain injury (TBI). The M1/M2 balance determines neurological outcomes, yet the mechanisms governing this polarization remain unclear. This study identifies neurokinin B (NKB) as a novel regulator of microglial M1/M2 polarization in TBI. Using a murine TBI model, we demonstrated significant upregulation of NKB and its receptor NK3R. Genetic knockdown of NKB enhanced functional recovery and shifted microglial polarization from the detrimental M1 to the beneficial M2 phenotype. Conversely, NKB administration promoted M1 activation while suppressing M2 markers in microglial cultures, potentially through inhibition of the STAT6 pathway. Overexpression of STAT6 reversed NKB's suppressive effects on M2 polarization, while NK3R antagonism with SB222200 promoted M2 polarization and improved functional outcomes. These findings establish NKB signaling as a key modulator of microglial dynamics after TBI, suggesting that targeting this pathway may promote neuroprotective M2 polarization while inhibiting damaging M1 responses. This dual regulation, combined with improved cognitive recovery, positions NKB as a promising target for developing novel TBI therapies aimed at modulating neuroinflammation.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102549"},"PeriodicalIF":2.7,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144829599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay of neuropeptide Y and autophagy in Alzheimer's disease: Therapeutic perspectives and mechanistic insights","authors":"Dhiraj Lanjewar,&nbsp;Raj Katariya,&nbsp;Vinita Kale,&nbsp;Brijesh Taksande,&nbsp;Milind Umekar,&nbsp;Madhura Vinchurney","doi":"10.1016/j.npep.2025.102547","DOIUrl":"10.1016/j.npep.2025.102547","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a progressive, chronic, neurodegenerative disorder involving cognitive impairment, neuronal loss, autophagy dysregulation, and toxic protein aggregates build-up, including amyloid-β plaques and hyperphosphorylated tau tangles. Autophagy dysregulation is a central driving force behind AD pathogenesis, interfering with the clearance of these aggregates and resulting in synaptic disruption and enhanced neurodegeneration. Neuropeptide Y (NPY) is abundantly present in the CNS. NPY has been identified as a promising candidate due to its neuropeptidergic activity. It plays a central role in regulating autophagy, anti-inflammation, and the induction of synaptic plasticity. NPY regulates the AMPA-mTOR pathway to restore cellular homeostasis and enhance neuronal survival through improved autophagic flux. It facilitates the clearance of aggregate proteins and dysfunctional cellular components, which lessen the signs of AD pathology. Moreover, NPY plays an important role in stabilizing the mitochondria and enhancing antioxidant action, in effect sustaining cognitive function. The modulatory influence of NPY on autophagy represents a potential novel direction in AD therapy, advanced delivery systems, such as nanoparticle-based carriers, offer promising targeted brain delivery mechanisms. However, clinical application is hindered by the need for a receptor-specific agonist to mitigate side effects and the lengthy trials necessary to assess long-term efficiency. Further research should aim to optimise NPY delivery and autophagy-targeted therapies to develop more effective treatments; such research challenges may position NPY as a breakthrough candidate for slowing cognitive and functional impairment in AD.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102547"},"PeriodicalIF":2.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144679854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irisin alleviates anxiety and deficits in fear extinction in PTSD within SPS mouse model","authors":"Xupei Xie ,&nbsp;Yandi Ding ,&nbsp;Qizhi Yan ,&nbsp;Jiadan Zhao ,&nbsp;Lingdi Zhang","doi":"10.1016/j.npep.2025.102537","DOIUrl":"10.1016/j.npep.2025.102537","url":null,"abstract":"<div><div>Post-Traumatic Stress Disorder (PTSD), a prevalent psychological disorder, emerges subsequent to a grave traumatic incident or a succession of such events. Irisin is expressed in brain regions such as the hippocampus and prefrontal cortex and is found to have a neuroprotective function by suppressing neuroinflammation through the AMPK pathway, demonstrating its potential in treating cognitive decline, having antidepressant effects, and intervening in stress-related disorders. This study aims to explore the potential therapeutic effects of irisin on PTSD, as well as investigate the underlying mechanisms. Results showed that SPS caused anxiety-like behaviors and deficit in fear memory extinction of the mice. These SPS-induced abnormalities of the mice were reversed by exogenous irisin treatment. However, the AMPK inhibitor abolished the protective effects of irisin, indicating that irisin's therapeutic effects on SPS mice were achieved by activating AMPK. Further biochemical experiments demonstrated that irisin could increase pAMPK levels and ameliorate the overexpression of NF-κB and its downstream factors, including inflammatory factors and neurotoxic mediators, in the hippocampus, frontal cortex, and amygdala of the SPS mice. These effects of irisin were also reversed by AMPK inhibitor. Cell experiments suggest that irisin exerts anti-inflammatory effects on BV2 cells (microglia) via the AMPK/NF-κB pathway and subsequently confers anti-inflammatory benefits while enhancing cell viability in PC12 cells. The cumulative results indicate that irisin can improve behavioral deficits induced by SPS in mice by exerting anti-neuroinflammation function, and this function may be associated with the modulation of AMPK/NF-κB pathway in microglia in the brain tissues including hippocampus, cerebral cortex, and amygdala.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"113 ","pages":"Article 102537"},"PeriodicalIF":2.5,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144653283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropeptide Y as a multifaceted modulator of neuroplasticity, Neuroinflammation, and HPA axis dysregulation: Perceptions into treatment-resistant depression","authors":"Priyanka Singanwad ,&nbsp;Amol Tatode ,&nbsp;Mohammad Qutub ,&nbsp;Brijesh Taksande ,&nbsp;Milind Umekar ,&nbsp;Rashmi Trivedi ,&nbsp;Tanvi Premchandani","doi":"10.1016/j.npep.2025.102538","DOIUrl":"10.1016/j.npep.2025.102538","url":null,"abstract":"<div><div>Treatment-resistant depression (TRD) is a severe neurobiological and clinical category in which common antidepressants do not induce an adequate response. Neuropeptide Y (NPY), a neuropeptide highly conserved through evolution, is known to be involved in the regulation of stress responses, emotional processing, neuroinflammation, and neuroplasticity. This review synthesizes the importance of NPY in TRD by describing NPY's physiological (central nervous system) functions and roles. Experimental data suggest that NPY is dysregulated in animal models of chronic stress and TRD, which include changes in hippocampal NPY signaling, neurotrophic factor expression, and HPA axis activity. Clinical studies have, in turn, shown decreased cerebrospinal NPY concentrations in TRD patients as well as decreased expression of NPY receptors in stress-related regions of their brains. Finally, we discuss new therapeutic avenues targeting NPY pathology, such as intranasal NPY administration and receptor-selective modulation. Thus, preclinical and clinical data jointly suggest that restoration of NPY signaling pathways might offer a novel and biologically grounded intervention for TRD.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102538"},"PeriodicalIF":2.5,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144632410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tauopathies: Emerging discoveries on tau protein, with a special focus on Alzheimer's disease","authors":"Aishwarya Hattiholi ,&nbsp;Harsha Hegde ,&nbsp;Suhas Kumar Shetty","doi":"10.1016/j.npep.2025.102536","DOIUrl":"10.1016/j.npep.2025.102536","url":null,"abstract":"<div><div>Tauopathies encompass a group of neurodegenerative disorders (NDDs) driven by the abnormal accumulation of mutated tau protein, leading to hyperphosphorylation, neuronal damage, and neuroinflammation. The protein plays essential roles in brain function but undergoes hyperphosphorylation and aggregation into toxic oligomers in NDDs. Recent research emphasizes the need to understand tau's post-translational modifications (PTMs) and their role in pathological states. Insights into tau's structure, isoform-specific properties, and aggregation mechanisms are critical for elucidating its propagation in neurodegeneration. Moreover, tau's potential as a biomarker and the development of targeted therapies to mitigate tauopathies, particularly in AD, remain promising avenues. However, many strategies targeted at tau have repeatedly failed, which continues the search for better alternatives. This review focuses on recent advances in tau research, highlighting its structural and functional characteristics, and roles in disease, that may be critical to understanding their implications for new therapeutic strategies. PTMs are important for the stable structure and physiological functions of a protein. However, dysfunctional PTMs are the leading causes of tau protein aggregation. The recent shift on tau hyperphosphorylation has resulted in many discoveries related to their functions in AD. Therapeutic strategies targeting phosphorylated tau are being extensively studied worldwide. This paper gives a comprehensive view on these aspects.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102536"},"PeriodicalIF":2.5,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144571243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynorphin B induces mitochondrial fragmentation in NSCLC through the PKD/DRP-1 signaling pathway","authors":"Yunxiao Li ,&nbsp;Bin Zhou ,&nbsp;Yuenan Yang ,&nbsp;Kexin Liu ,&nbsp;Shichao Zhou","doi":"10.1016/j.npep.2025.102535","DOIUrl":"10.1016/j.npep.2025.102535","url":null,"abstract":"<div><div>Mitochondrial fragmentation and impairment are essential targets for therapeutic approach for non-small cell lung cancer (NSCLC), given their significant contributions to the persistence and progression of malignant cells. Dynorphin B (Dyn B), an endogenous opioid peptide, has been demonstrated for its involvement in an extensive array of cellular activities; however, its specific functions and mechanisms within the context of cancer remain largely undefined. To address this, we employed NCI-H2087 NSCLC cells treated with Dyn B (0.01–100 μM) and utilized lactate dehydrogenase (LDH) release and γ-glutamyl transpeptidase (GPT) activity assays to evaluate cytotoxicity. Mitochondrial function was assessed via Complex I activity assays, adenosine triphosphate (ATP) production measurements, and MitoSOX Green staining for reactive oxygen species (ROS). MitoTracker Red staining with ImageJ quantification characterized mitochondrial morphology, while Western blot analysis probed phosphorylation of dynamin-related protein 1 (DRP1) and protein kinase D (PKD). Lentiviral shRNA-mediated PKD silencing was used to validate functional rescue of mitochondrial dynamics. This investigation reveals that Dyn B induces cytotoxic effects in NCI-H2087 NSCLC cells by facilitating mitochondrial dysfunction and fragmentation. Treatment with Dyn B resulted in a significant augmentation of LDH and elevated GPT activity, indicating cellular injury. Additionally, Dyn B compromised mitochondrial functionality by reducing Complex I activity, diminishing ATP synthesis, and promoting mitochondrial ROS generation. Mechanistically, Dyn B triggered mitochondrial fragmentation through activation of DRP1 and PKD, without affecting protein kinase C (PKC). Silencing of PKD reversed Dyn B–induced mitochondrial fragmentation and restored mitochondrial functionality. These findings underscore the promising role of Dyn B as a prospective therapeutic agent in NSCLC, targeting mitochondrial dynamics via the PKD-DRP1 signaling pathway.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102535"},"PeriodicalIF":2.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144517632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effect of Ac-SDKP peptide in SH-SY5Y cells and rat model of Parkinson's disease against 6-OHDA-induced oxidative stress and ER stress","authors":"Maryam Kamarehei ,&nbsp;Hamid Zahednasab","doi":"10.1016/j.npep.2025.102534","DOIUrl":"10.1016/j.npep.2025.102534","url":null,"abstract":"<div><div>Oxidative stress and endoplasmic reticulum (ER) stress are key contributors to the pathogenesis of neurodegenerative diseases, including Parkinson's disease (PD), for which no definitive cure currently exists. This study investigated the neuroprotective potential of the <em>N</em>-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) tetrapeptide in both in vitro and in vivo PD models. In cell-based analyses, pre-treatment with 20 nM Ac-SDKP provided significant protection against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in SH-SY5Y cells. In vivo, the neuroprotective potential of the peptide was also supported through daily administration of rats with Ac-SDKP (800 μg/kg) after 6-OHDA lesioning, which unveiled a series of significant observations. Treated animals demonstrated highly preserved dopaminergic neurons through reduced activation of apoptotic markers such as caspase-3 and caspase-12. In addition to cytoprotection, Ac-SDKP also produced striking behavioral improvement. Treated animals exhibited improved motor coordination and ability on spatial memory tasks, as well as the significant attenuation of anxiety-like and depressive-like behaviors. Such behavioral improvement is probable because Ac-SDKP possesses the ability to modulate several pathological features of PD. In fact, the peptide was able to decrease oxidative stress, diminish ER stress, and inhibit neuroinflammatory signaling. Collectively, these findings position Ac-SDKP as a promising neuroprotection candidate, and as a candidate with potential to be developed as a multifactorial treatment for the complex pathophysiology of PD.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102534"},"PeriodicalIF":2.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis","authors":"Susana Aideé González-Chávez ,&nbsp;Eduardo Chaparro-Barrera ,&nbsp;Mario Loya-Rivera ,&nbsp;Alejandra Jazmín Rodríguez-Castillo ,&nbsp;Rodrigo Prieto-Carrasco ,&nbsp;Renato J. Aguilera ,&nbsp;Ana P. Betancourt ,&nbsp;Jonathon E. Mohl ,&nbsp;Daniel Alberto Ruizesparza-Hinojos ,&nbsp;Sergio de Jesús Ramírez-Pérez ,&nbsp;Mercedes Bermúdez ,&nbsp;César Pacheco-Tena","doi":"10.1016/j.npep.2025.102533","DOIUrl":"10.1016/j.npep.2025.102533","url":null,"abstract":"<div><h3>Background</h3><div>Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by immune dysregulation and joint destruction. Cellular senescence has been implicated in the progression of RA through the senescence-associated secretory phenotype (SASP), yet its molecular links to inflammation remain unclear. Rapamycin, an mTOR inhibitor with anti-inflammatory and anti-senescence properties, provides a valuable tool for exploring these mechanisms.</div></div><div><h3>Objective</h3><div>To investigate the link between senescence and inflammation in a murine model of RA by comparing the transcriptome of diseased joints in rapamycin-treated and untreated mice.</div></div><div><h3>Methods</h3><div>Collagen-induced arthritis was established in DBA/1 mice, followed by 40 days of rapamycin treatment. RNA sequencing and bioinformatic analyses were performed to identify differentially expressed genes and altered signaling pathways. RT-qPCR and immunohistochemistry validated candidate genes. Functional assays were conducted in fibroblast-like synoviocytes (FLS) following <em>Npy</em> silencing.</div></div><div><h3>Results</h3><div>Rapamycin treatment reduced the incidence and severity of arthritis while modulating senescence- and autophagy-related pathways. Transcriptomic analysis identified neuropeptide Y (<em>Npy</em>) as a differentially expressed gene linking senescence and inflammation, with reduced protein levels following rapamycin treatment, similar to TNF and β-galactosidase. NPY receptor expression (<em>Npy1r</em> and <em>Npy2r</em>) and autophagy-related genes (<em>Sirt1</em>, <em>Sirt6</em>, and <em>Lc3b</em>) were also modulated in vivo. In vitro, <em>Npy</em> silencing in FLS significantly reduced the expression of the SASP cytokines <em>Tnfa</em>, <em>Il1b</em>, and <em>Il6</em>, downregulated <em>Npy1r</em> and <em>Npy2r</em>, and increased <em>Sirt1</em> expression.</div></div><div><h3>Conclusion</h3><div>This study identifies <em>Npy</em> as a modulator of inflammation and senescence-related pathways in arthritis. Its regulation by rapamycin and impact on sirtuins, autophagy, and NPY receptor expression suggest a broader role in RA pathogenesis.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102533"},"PeriodicalIF":2.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144308168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of oxytocin on behavior and neurotrophic factors in the brain of aged female rats exposed to chronic social isolation","authors":"Helin Demirtas ,&nbsp;Burcu Acikgoz ,&nbsp;Ayca Arslankiran ,&nbsp;Bahar Dalkiran ,&nbsp;Amac Kiray ,&nbsp;Muge Kiray ,&nbsp;Ayfer Dayi ,&nbsp;Ilkay Aksu","doi":"10.1016/j.npep.2025.102532","DOIUrl":"10.1016/j.npep.2025.102532","url":null,"abstract":"<div><div>This study aimed to investigate the effects of social isolation stress and intranasally administered oxytocin on physiological and behavioral alterations during aging in rats. A total of 28, aged female Sprague-Dawley rats were allocated into four groups: control (C), social isolation (SI), oxytocin (O), and oxytocin+social isolation (OI). Animals in the SI and OI groups were housed in individual cages for four weeks. Intranasal oxytocin (2 μg/kg/day) was administered to the O and OI groups 14 times during the third and fourth weeks of the study. Behavioral assessments were conducted. Levels of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) were measured. In the Morris water maze test, all groups demonstrated improved learning performance, reflected by a progressive reduction in the time taken to locate the hidden platform. The three-chamber sociability test revealed that sociability was significantly impaired in the SI group but preserved in the O, OI, and C groups. VEGF levels in the prefrontal cortex were significantly reduced in the SI group compared to all other groups. Notably, VEGF levels were higher in the OI group than in the SI group. Hippocampal neuron density was lower in the SI group but was preserved in the OI group, suggesting a neuroprotective effect of oxytocin. These findings highlight the protective roles of oxytocin and sociability against the detrimental effects of chronic social isolation, particularly in preserving hippocampal neuron density and maintaining sociability and learning. Further research is needed to elucidate the molecular and behavioral mechanisms underlying these effects.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102532"},"PeriodicalIF":2.5,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}