Journal of neuroimmunology最新文献

{"title":"Greater fatigue, disturbed sleep, persistent memory problems, and reduced CD4+ T cell and B cell percentages in adults with a history of methamphetamine dependence","authors":"Elizabeth K. Wood ,&nbsp;Elaine Huang ,&nbsp;Emily R. Sano ,&nbsp;Jennifer M. Loftis","doi":"10.1016/j.jneuroim.2025.578567","DOIUrl":"10.1016/j.jneuroim.2025.578567","url":null,"abstract":"<div><div>Methamphetamine (MA) dependence is associated with immunotoxicity and high rates of neuropsychiatric impairments that persist into remission. Although there are currently no FDA-approved pharmacotherapies for MA use disorders, preclinical and clinical studies are beginning to test interventions that directly impact immune signaling. This study was conducted to investigate the relative contribution of immune cell function to the neuropsychiatric sequelae associated with MA dependence and remission. Participants were enrolled into the following study groups: i) control (CTL) group (<em>n</em> = 62): adults with no lifetime history of dependence on any substance other than nicotine or caffeine; and ii) MA group (<em>n</em> = 98) [MA-remission group (<em>n</em> = 55): adults in remission ≥1 month and ≤ 6 months and MA-active group (<em>n</em> = 43): adults actively using MA and meeting criteria for MA dependence]. Participants completed a clinical interview, urine drug analysis, blood sample collection, and questionnaires. Peripheral blood mononuclear cells were analyzed by flow cytometry. Results suggest that early remission from MA dependence is associated with increased fatigue and persistent sleep and prospective and retrospective memory problems, along with reduced B and CD4⁺ T cell percentages, compared to the CTL group. Preliminary findings support the hypothesis that the immune system modulates the sleep impairments associated with drug actions and provide implications for future research studies and treatment approaches.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"402 ","pages":"Article 578567"},"PeriodicalIF":2.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxocara canis-originated recombinant C-type lectin improves the disability scores of experimental autoimmune encephalomyelitis in murine in vivo models","authors":"Mahsa Shahbakhsh ,&nbsp;Fateme Jalousian ,&nbsp;Seyed Hossein Hosseini ,&nbsp;Abdorreza Naser Moghadasi ,&nbsp;Parviz Shayan ,&nbsp;Samad Farashi Bonab ,&nbsp;Parmida Malekzade ,&nbsp;Mohammad Vojgani ,&nbsp;Mahya Lalehpour","doi":"10.1016/j.jneuroim.2025.578569","DOIUrl":"10.1016/j.jneuroim.2025.578569","url":null,"abstract":"<div><h3>Background</h3><div>The recombinant C-type lectin protein (r-CTL) derived from <em>Toxocara canis</em> larvae is thought to play a role in promoting regulatory T cell-dominant immune responses in toxocariasis. This study aimed to highlight the therapeutic potential of the r-CTL protein in improving the disability scores of EAE by enhancing the Foxp3⁺-CD25⁺ T cells population.</div></div><div><h3>Methods</h3><div>The r-CTL was expressed in prokaryotic systems and purified using Ni-NTA spin columns. Balb/C57 mice were divided into six groups, with EAE induced in four of them, excluding the healthy control group and the group receiving only r-CTL treatment. Group I (<em>n</em> = 10) received r-CTL treatment post EAE induction, Group II (n = 10) underwent EAE induction only, Group III (<em>n</em> = 5) received treatment with <em>E. coli</em> lysate proteins containing <em>E. coli</em> BL21 and plasmid pET32a without r-CTL after EAE induction, Group IV (n = 5) received sterile PBS after EAE induction, Group V (n = 5) served as the healthy control group, and Group VI (n = 5) received only r-CTL treatment.</div></div><div><h3>Results</h3><div>The study's findings revealed that r-CTL treatment significantly decreased disability scores in EAE-induced mice. There was a notable increase in the population of CD4+, CD25+, FOXP3+ regulatory T cells following r-CTL treatment. The gene expression levels of IL-10, FOXP3, and GATA3 were significantly elevated in the r-CTL treated group, while the expression of T-bet and RORγ genes was reduced. Treatment with r-CTL significantly mitigated cell infiltration and demyelination in both the spinal cord and brain.</div></div><div><h3>Conclusion</h3><div>In conclusion, the observed improvements in disability scores in the EAE mouse model suggest that r-CTL protein could be a potential new treatment approach worth further investigation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"402 ","pages":"Article 578569"},"PeriodicalIF":2.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of altered oxi-inflammasome activity in the immunobiology of inflammatory neuropathies","authors":"Madhu Nagappa ,&nbsp;Sandipan Mondal ,&nbsp;Srinath Rajeevan ,&nbsp;B. Pradeepkumar ,&nbsp;Vamsi Chalasani ,&nbsp;Saikat Dey ,&nbsp;Gopika Suresh Babu ,&nbsp;Aritrani Sarkar ,&nbsp;Lakshminarayanapuram G. Viswanathan ,&nbsp;Doniparthi V. Seshagiri ,&nbsp;V.S. Binu ,&nbsp;Monojit Debnath","doi":"10.1016/j.jneuroim.2025.578556","DOIUrl":"10.1016/j.jneuroim.2025.578556","url":null,"abstract":"<div><h3>Objectives</h3><div>Inflammasome plays a significant role in inflammatory responses. The role of inflammasome and its interactions with oxidative stress markers has not been examined in inflammatory neuropathies like Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). This study aims to explore the roles of inflammasome and oxidative stress pathways in inflammatory neuropathies.</div></div><div><h3>Methods</h3><div>This case-controlled study comprised patients with inflammatory neuropathies (<em>n</em> = 60, GBS = 44, CIDP = 16) and age- and gender-matched healthy controls (n = 60). The expressions of inflammasome-related genes (<em>Nlrp3, Casp1,</em> and <em>Il1b)</em> were quantified along with the plasma levels of malondialdehyde (MDA), the end product of lipid peroxidation in all study participants.</div></div><div><h3>Results</h3><div>The expressions of <em>Nlrp3</em> (<em>p</em> = 0.0083) and <em>Casp1</em> (<em>p</em> = 0.0007) genes were significantly up-regulated in GBS patients compared to controls. The plasma MDA levels were also markedly higher in GBS patients than in controls (<em>p</em> = 0.029). The gene expression levels of <em>Nlrp3, Casp1,</em> and <em>Il1b</em> and plasma MDA levels were comparable between CIDP patients and healthy controls. There were no correlations between the expressions of the studied genes and MDA levels with the clinical scores of GBS.</div></div><div><h3>Conclusion</h3><div>The up-regulated expression of <em>Nlrp3</em> and <em>Casp1</em> genes and increased levels of MDA suggest the presence of an activated oxi-inflammatory pathway in GBS. These findings provide a new dimension to the current understanding of the immuno-pathogenesis of GBS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578556"},"PeriodicalIF":2.9,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response of refractory residual ocular symptoms to efgartigimod in generalized myasthenia gravis: A real-world case series","authors":"Dingxian He ,&nbsp;Yufan Zhou ,&nbsp;Yexin Zhang ,&nbsp;Jialong Zhang ,&nbsp;Chong Yan ,&nbsp;Sushan Luo ,&nbsp;Chongbo Zhao ,&nbsp;Jianying Xi","doi":"10.1016/j.jneuroim.2025.578558","DOIUrl":"10.1016/j.jneuroim.2025.578558","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the efficacy of efgartigimod (EFG) in treating residual ocular symptoms in myasthenia gravis (MG) patients with acetylcholine receptor antibodies (AChR-Ab).</div></div><div><h3>Methods</h3><div>Five MG patients with refractory residual ocular symptoms treated with EFG at Huashan Hospital were included. The demographic and clinical information was collected, and MG Activities of Daily Living (MG-ADL) scores and Quantitative Myasthenia Gravis (QMG) scores was elevated weekly during the 8-week follow up period. The time to reach minimal symptom expression (MSE) was also recorded.</div></div><div><h3>Results</h3><div>After a single cycle of EFG infusion, all five patients showed response in MG-ADL (≥2 points reduction), and three patients in QMG score (≥3 points reduction). The mean ± SD MG-ADL scores decreased significantly from 5.0 ± 1.0 at baseline to 1.8 ± 1.1 at weak 4 (<em>p</em> = 0.0027) and 1.8 ± 0.5 at weak 6 (p = 0.0027). The mean ± SD QMG score decreased from 5.8 ± 0.5 at baseline to 2.4 ± 1.7 at week 4 (<em>p</em> = 0.1357) and 1.0 ± 0.7 at week 6 (<em>p</em> = 0.0076). The proportions of patients reaching MSE at week 4, 6 and 8 were 20 % (1/5), 20 % (1/5), and 60 % (3/5), respectively.</div></div><div><h3>Conclusions</h3><div>AChR-Ab+ MG patients with residual and refractory ocular symptoms could benefit from EFG treatment, while the duration of efficacy varied in individuals.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578558"},"PeriodicalIF":2.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143479653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of rituximab on antibody-positive small fiber neuropathy: A series of 5 cases","authors":"Amanda C.Y. Chan ,&nbsp;R. Shahana ,&nbsp;Kewin T.H. Siah ,&nbsp;Nicholas Foo ,&nbsp;Yee-Cheun Chan ,&nbsp;Kay W.P. Ng ,&nbsp;Amy M.L. Quek ,&nbsp;Rahul Rathakrishnan ,&nbsp;Shi-Yang Ng ,&nbsp;Herbert Schwarz ,&nbsp;Anselm Mak ,&nbsp;Vijay Kumar Sharma","doi":"10.1016/j.jneuroim.2025.578559","DOIUrl":"10.1016/j.jneuroim.2025.578559","url":null,"abstract":"<div><h3>Background &amp; aims</h3><div>We evaluated the efficacy of rituximab in patients with anti-TS-HDS, anti-FGFR3 and anti-plexin D1 small fiber neuropathy (SFN) who failed to respond to conventional treatments and immunotherapy.</div></div><div><h3>Methods</h3><div>We reviewed 111 patients diagnosed with SFN - 83 definite SFN, 9 had positive antibody titers towards TS-HDS, FGFR3 or plexin-D1 and received symptomatic treatment, in addition to trials of intravenous immunoglobulin (IVIg) and/or corticosteroids. Five patients who failed to respond were offered rituximab (two intravenous 1 g infusions, two weeks apart). Clinical parameters and questionnaires were compared.</div></div><div><h3>Results</h3><div>Two patients were positive for anti-TS-HDS, one for anti-plexin D1 and two for anti-FGFR3 antibodies. Therapeutic efficacy was assessed by circulating CD19⁺ B cell levels with flow cytometry. Clinical questionnaires, including Visual Analogue Scale (VAS), Rasch Transformed 13-item SFN Symptom Inventory Quotient (RT-SFN-SIQ), Small Fiber Neuropathy-specific Rasch-built overall disability scale (SFN-RODS) and the Composite Autonomic Symptom Scale (COMPASS-31) were obtained prior to rituximab infusion, and at 4 weeks and 4 months post-infusion. Significantly improved VAS was seen at 4 months after rituximab, while a trend towards improvement was seen in RT-SFN-SIQ, and SFN-RODS. COMPASS-31 score remained static.</div></div><div><h3>Interpretation</h3><div>This study illustrates the efficacy and potential role of anti-CD20 monoclonal antibody in antibody-associated immune SFN, especially in those who fail to respond to IVIg or corticosteroid. Further randomized controlled trials and larger prospective studies are needed to determine the effectiveness and safety of Rituximab in seropositive patients with SFN.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578559"},"PeriodicalIF":2.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzoylacetonitrile as a novel anti-inflammatory compound on attenuating microglia and encephalitogenic T cell activation in experimental autoimmune encephalomyelitis","authors":"Ping-Chang Kuo ,&nbsp;Zixuan Zhao ,&nbsp;Barbara A. Scofield ,&nbsp;Hallel C. Paraiso ,&nbsp;I-Chen Ivorine Yu ,&nbsp;Dennis A. Brown ,&nbsp;Jui-Hung Jimmy Yen","doi":"10.1016/j.jneuroim.2025.578557","DOIUrl":"10.1016/j.jneuroim.2025.578557","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is an autoimmune disorder and characterized by immune-mediated neuroinflammation and demyelination triggered by the CNS resident immune cells, microglia (MG), and CNS infiltrating pathogenic T cells. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS, and MG activation and pathogenic Th1/Th17 cell infiltration is responsible for EAE development and progression. We previously demonstrated that benzoylacetonitriles exerted neuro-immunomodulatory activity and identified compound 7a (referred to henceforth as BTA) as promising analog. Here, we investigated whether BTA possessed effects on modulating inflammatory responses in EAE and assessed its effects on MG activation and pathogenic Th1/Th17 differentiation and CNS infiltration in EAE. Our results showed BTA ameliorated disease severity in the chronic C57BL/6 EAE model. Further studies demonstrated BTA suppressed MG activation, attenuated CNS Th1/Th17 infiltration, and inhibited peripheral Th1/Th17 differentiation in EAE. Using protein array, we confirmed BTA inhibited MG activation by suppressing inflammatory cytokines/chemokine production. Furthermore, BTA suppressed Th1/Th17 polarization <em>in vitro</em>, indicating a direct suppressive effect of BTA on Th1/Th17 differentiation. Finally, our results showed that BTA prevented disease relapse in the relapsing-remitting SJL EAE model. In conclusion, our study demonstrates BTA possessed protective and therapeutic effects by ameliorating disease severity in the chronic EAE and mitigating relapse in the relapsing-remitting EAE, respectively. Further analysis revealed BTA exerted effects on inhibiting MG activation and Th1/Th17 differentiation, demonstrated by <em>in vivo</em> and <em>in vitro</em> studies. Altogether, our results suggest the benzoylacetonitrile scaffold could be developed as a novel therapeutic agent for MS/EAE treatment.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578557"},"PeriodicalIF":2.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sugar utilization by microglia in Alzheimer's disease","authors":"Kaitlyn M. Marino ,&nbsp;Daniel C. Shippy ,&nbsp;Tyler K. Ulland","doi":"10.1016/j.jneuroim.2025.578552","DOIUrl":"10.1016/j.jneuroim.2025.578552","url":null,"abstract":"<div><div>Diabetes is a major risk factor for Alzheimer's disease (AD), yet the effect of specific carbohydrate sources in the diet on AD pathology remains unclear. The primary neuroimmune cell, microglia, undergo a metabolic shift during neuroinflammation associated with AD pathology. We utilized existing gene expression data and identified changes in sugar transporters (increased <em>Slc2a1</em> (glucose) and decreased <em>Slc2a5</em> (fructose) expression). To examine gene expression with respect to primary sugar source, N9 cells, a mouse microglia cell line, were cultured in glucose or fructose supplemented media and stimulated with lipopolysaccharide (LPS). RNA-sequencing analyses indicated significant changes between control and sugar supplemented media and several differentially expressed genes between glucose and fructose media. Concurrently, 5XFAD mice received equicaloric diets with specific carbohydrate sources: dextrose or fructose. Regardless of diet, sex, or genotype, all mice developed high blood sugar levels; confocal microscopy analyses indicated similar amyloid plaque burden and microglial response relative to the control diet, but there was a change in the microglial response between dextrose and fructose fed mice. Overall, these data indicate microglia preferentially express sugar transporters and sugar source may influence microglial reactivity in response to plaque pathology.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578552"},"PeriodicalIF":2.9,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunotherapy challenges and potential role of unclassified antibodies in complex autoimmune encephalitis","authors":"Shampa Ghosh ,&nbsp;Rakesh Bhaskar ,&nbsp;Krishna Kumar Singh ,&nbsp;Jitendra Kumar Sinha","doi":"10.1016/j.jneuroim.2025.578555","DOIUrl":"10.1016/j.jneuroim.2025.578555","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"401 ","pages":"Article 578555"},"PeriodicalIF":2.9,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD47-blocking antibody interferes with neutrophil extracellular traps formation after spinal cord injury to reduce spinal cord edema","authors":"Yuhang Diao,&nbsp;Mingyu Hao,&nbsp;Minghao Xie,&nbsp;Xiaojun Hu,&nbsp;Rui Tan,&nbsp;Zhitan Wang,&nbsp;Hongtao Rong,&nbsp;Tao Zhu","doi":"10.1016/j.jneuroim.2025.578553","DOIUrl":"10.1016/j.jneuroim.2025.578553","url":null,"abstract":"<div><h3>Objective</h3><div>Our goal was to investigate the role of neutrophil extracellular traps (NETs) in the disruption of the blood-spinal cord barrier (BSCB) following spinal cord injury (SCI) and to evaluate the therapeutic efficacy of CD47-blocking antibodies in mitigating the disruption.</div></div><div><h3>Methods</h3><div>We utilized Evans blue extravasation to evaluate BSCB permeability and immunofluorescence to evaluate the formation of NETs and the expression of ZO-1, CD31, S100A8/A9, CD68, GFAP, Iba-1, and NeuN. Spinal cord edema was quantified by comparing the dry and wet weights of tissue samples. We used enzyme-linked immunosorbent assay (ELISA) to evaluate inflammatory factors, including IL-1β, IL-6, and TNF-α. Changes in genes associated with NET formation were identified by mRNA sequencing. Activation of the TLR4-NF-κB-MMP2/MMP9 signaling pathway was examined via Western blot analysis. Limb function was evaluated using the Basso Mouse Scale (BMS) to assess motor function.</div></div><div><h3>Results</h3><div>We observed massive aggregation of neutrophils and the formation of neutrophil extracellular traps (NETs) after spinal cord injury. The use of CD47-blocking antibodies reduced NET formation, mitigated S100A8/A9 production, attenuated BSCB injury, decreased inflammatory cell infiltration, alleviated spinal cord edema, and minimized neuronal death at the site of injury. Furthermore, these antibodies suppressed activation of the TLR4-NF-κB-MMP2/MMP9 signaling pathway.</div></div><div><h3>Conclusion</h3><div>The use of CD47-blocking antibodies post-SCI resulted in reduced NET formation. By suppressing the TLR4-NF-κB-MMP2/MMP9 signaling pathway, these antibodies contributed to the preservation of blood-spinal cord barrier (BSCB) integrity, highlighting their potential as a therapeutic strategy for SCI.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"400 ","pages":"Article 578553"},"PeriodicalIF":2.9,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143402762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Traditional pediatric massage exerted an antidepressant effect and activated IGF-1/Nrf2 pathway in CUMS-exposed adolescent rats","authors":"Xingxing Zhang ,&nbsp;Que Liu ,&nbsp;Siyuan Li ,&nbsp;Rong Wu ,&nbsp;Ying Xiong ,&nbsp;Yuhang Wang ,&nbsp;Yun Gu ,&nbsp;Zhixiu Song ,&nbsp;Jiaxuan Gong ,&nbsp;Shaoyun Zhao","doi":"10.1016/j.jneuroim.2025.578554","DOIUrl":"10.1016/j.jneuroim.2025.578554","url":null,"abstract":"<div><div>The activation of insulin-like growth factor-1 (IGF-1)/nuclear factor-erythroid 2 related factor 2 (Nrf2) pathway contributes to enhance anti-inflammatory M2 microglia polarization and inhibit proinflammatory M1 microglia polarization, which is essential to resist neuroinflammation and thus resist depression. The prevalence of depression is high in adolescents, who are hypersensitive to chronic stress. Traditional pediatric massage (TPM) can effectively relieve depression. In this study, we investigated the action mechanism of TPM on preventing depression-like behaviors in adolescent rats exposed to chronic unpredictable mild stress (CUMS). In this investigation, we employed several behavioral tests and detections, including western blotting, immunofluorescence staining and RT-qPCR. The findings of this study demonstrated that TPM had an effectively antidepressant effect, maintained microglia polarization homeostasis and resisted neuroinflammation in the hippocampus in CUMS-exposed adolescent rats. With the treatment of picropodophyllin, the inhibitor of IGF-1 receptor, the antidepressant effect of TPM was blocked, along with inhibited IGF-1/Nrf2 pathway which were closely related with anti-inflammatory and anti-ferroptosis actions. The results suggest that TPM enhanced the resilience of adolescent rats to CUMS and exerted an antidepressant effect partially via activating IGF-1/Nrf2 pathway.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"400 ","pages":"Article 578554"},"PeriodicalIF":2.9,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}