Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology最新文献

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Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling. 甲酰基肽受体-2抑制自噬通过PI3K/Akt信号传导促进人胶质母细胞瘤细胞的迁移和侵袭
IF 3.5
Zhenzhao Luo, Deyong Kong, Guangjian Qi, Chao Zheng, Wushi Zhao, Zhongxin Lu
{"title":"Formyl Peptide Receptor-2-Suppressed Autophagy Promotes the Migration and Invasion of Human Glioblastoma Cells Through PI3K/Akt Signaling.","authors":"Zhenzhao Luo, Deyong Kong, Guangjian Qi, Chao Zheng, Wushi Zhao, Zhongxin Lu","doi":"10.1007/s11481-026-10284-z","DOIUrl":"10.1007/s11481-026-10284-z","url":null,"abstract":"<p><p>Formyl peptide receptor-2 (FPR2) belongs to the G protein-coupled receptor (GPCR) family and plays a critical role in the development of various tumors. However, the roles and mechanisms of FPR2 in glioblastoma (GBM) remain poorly understood. In this study, we observed significant upregulation of FPR2 in glioma cell lines and tissues, and elevated FPR2 expression levels are correlated with poor patient survival. Furthermore, we found that FPR2 suppresses the autophagy mediated by BECN1 and ATG5 in GBM cells. Using Western blot analysis, we revealed that FPR2 regulates GBM cell invasion via the PI3K/AKT signaling pathway. Additionally, we demonstrated that knocking down FPR2 expression in GBM cells reduced tumor cell migration and invasion in vitro and tumor growth in vivo. The inhibition of FPR2 led to cell cycle arrest at the G2/M phase and increased apoptosis. Finally, our findings indicate that FPR2 may prevent autophagy-induced epithelial‒mesenchymal transition (EMT)-like changes by preventing autophagy-induced degradation of Snail. Our findings suggest that FPR2 promotes GBM cell migration and invasion through the inhibition of autophagy and the activation of the PI3K/AKT signaling pathway, highlighting the potential of inducing autophagy as a therapeutic approach to inhibit invasion in GBM with high FPR2 expression.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147391811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Melatonin Mitigates Central Sensitization and Nociplastic Pain in Spinal Cord and Dorsal Root Ganglia of FM Rat Model: Modulation of SIRT1/PGC-1α/MAPK/NF-κB Signaling. 褪黑素减轻FM大鼠脊髓和背根神经节中枢致敏和伤害性疼痛:SIRT1/PGC-1α/MAPK/NF-κB信号的调节
IF 3.5
Jehad Osama, Amira A El-Gazar, Ghada M Ragab, Nesrine S El-Sayed, Ahmed S Kamel
{"title":"Melatonin Mitigates Central Sensitization and Nociplastic Pain in Spinal Cord and Dorsal Root Ganglia of FM Rat Model: Modulation of SIRT1/PGC-1α/MAPK/NF-κB Signaling.","authors":"Jehad Osama, Amira A El-Gazar, Ghada M Ragab, Nesrine S El-Sayed, Ahmed S Kamel","doi":"10.1007/s11481-025-10274-7","DOIUrl":"10.1007/s11481-025-10274-7","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"12"},"PeriodicalIF":3.5,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12904926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
EcoHIV Infection Disrupts Dopamine and Serotonin Transporter Function, Altering Release Dynamics in C57BL/6J Mice. EcoHIV感染破坏多巴胺和血清素转运蛋白功能,改变C57BL/6J小鼠的释放动力学。
IF 3.5
Jun Zhu, Carles Moreno, Ana C Jimenez Torres, Sarah E Davis, Abagail B Cirincione, Sanjay B Maggirwar
{"title":"EcoHIV Infection Disrupts Dopamine and Serotonin Transporter Function, Altering Release Dynamics in C57BL/6J Mice.","authors":"Jun Zhu, Carles Moreno, Ana C Jimenez Torres, Sarah E Davis, Abagail B Cirincione, Sanjay B Maggirwar","doi":"10.1007/s11481-026-10280-3","DOIUrl":"10.1007/s11481-026-10280-3","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"11"},"PeriodicalIF":3.5,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12894441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146159550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Beta-lactam Antibiotic Cefepime Attenuates Lipopolysaccharide-induced Pain and Depression By Modulating Inflammatory Response and Astroglial Glutamate Transporter in Mice. 内酰胺类抗生素头孢吡肟通过调节小鼠炎症反应和星形胶质谷氨酸转运蛋白减轻脂多糖诱导的疼痛和抑郁。
IF 3.5
Amna Khan, Patrick J Ronan, Shafiqur Rahman
{"title":"Beta-lactam Antibiotic Cefepime Attenuates Lipopolysaccharide-induced Pain and Depression By Modulating Inflammatory Response and Astroglial Glutamate Transporter in Mice.","authors":"Amna Khan, Patrick J Ronan, Shafiqur Rahman","doi":"10.1007/s11481-026-10279-w","DOIUrl":"https://doi.org/10.1007/s11481-026-10279-w","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"10"},"PeriodicalIF":3.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146108950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Low-dose IL-2 Ameliorates Experimental Autoimmune Myasthenia Gravis in Rats by Restoring the CD4-positive Helper T-cell Balance Via the JAK/STAT5 Pathway. 低剂量IL-2通过JAK/STAT5通路恢复cd4阳性辅助性t细胞平衡改善实验性自身免疫性重症肌无力
IF 3.5
Shanshan Peng, Xiaotong Kong, Wenqi Tian, Fanfan Xu, Hanlu Cai, Fei Wu, Ying Li, Guanghao Xin, Jingyan Niu, Yingjie Ren, Lei Li, Jianjian Wang, Huixue Zhang, Lihua Wang
{"title":"Low-dose IL-2 Ameliorates Experimental Autoimmune Myasthenia Gravis in Rats by Restoring the CD4-positive Helper T-cell Balance Via the JAK/STAT5 Pathway.","authors":"Shanshan Peng, Xiaotong Kong, Wenqi Tian, Fanfan Xu, Hanlu Cai, Fei Wu, Ying Li, Guanghao Xin, Jingyan Niu, Yingjie Ren, Lei Li, Jianjian Wang, Huixue Zhang, Lihua Wang","doi":"10.1007/s11481-025-10276-5","DOIUrl":"10.1007/s11481-025-10276-5","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"9"},"PeriodicalIF":3.5,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146094992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exploratory Cohort Study of Depressive Symptoms in South Africans with HIV-1 Subtype C: Associations with Kynurenine Pathway Metabolites and Inflammatory Markers. 南非HIV-1亚型C患者抑郁症状的探索性队列研究:与犬尿氨酸途径代谢物和炎症标志物的关联
IF 3.5
Monray Edward Williams, Lusilda Schutte, Levanco K Asia, Marié P Wissing, Esmé Jansen van Vuren
{"title":"Exploratory Cohort Study of Depressive Symptoms in South Africans with HIV-1 Subtype C: Associations with Kynurenine Pathway Metabolites and Inflammatory Markers.","authors":"Monray Edward Williams, Lusilda Schutte, Levanco K Asia, Marié P Wissing, Esmé Jansen van Vuren","doi":"10.1007/s11481-025-10278-3","DOIUrl":"10.1007/s11481-025-10278-3","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"8"},"PeriodicalIF":3.5,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12830437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146031909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction: PKR Inhibition Prevents Neuroinflammation and Rescues Depressive‑Like Behaviors Via BDNF/TrkB Signaling. 修正:PKR抑制通过BDNF/TrkB信号阻止神经炎症和拯救抑郁样行为。
IF 3.5
Yue Hu, Tahir Ali, Shengnan Mou, Qichao Gong, Ruyan Gao, Yanhua Luo, Shupeng Li, Li Ling, Liangliang Hao
{"title":"Correction: PKR Inhibition Prevents Neuroinflammation and Rescues Depressive‑Like Behaviors Via BDNF/TrkB Signaling.","authors":"Yue Hu, Tahir Ali, Shengnan Mou, Qichao Gong, Ruyan Gao, Yanhua Luo, Shupeng Li, Li Ling, Liangliang Hao","doi":"10.1007/s11481-025-10277-4","DOIUrl":"https://doi.org/10.1007/s11481-025-10277-4","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"7"},"PeriodicalIF":3.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145992298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Repositioning of Alogliptin to Mitigate Secondary Injury Induced by Repetitive TBI: Potential Role of its Antioxidant and Anti- Inflammatory Effects. 阿格列汀重新定位以减轻重复性脑损伤引起的继发性损伤:其抗氧化和抗炎作用的潜在作用。
IF 3.5
Hossam A Raslan, Haidy E Michel, Esther T Menze, Amira A El-Gazar
{"title":"Repositioning of Alogliptin to Mitigate Secondary Injury Induced by Repetitive TBI: Potential Role of its Antioxidant and Anti- Inflammatory Effects.","authors":"Hossam A Raslan, Haidy E Michel, Esther T Menze, Amira A El-Gazar","doi":"10.1007/s11481-025-10271-w","DOIUrl":"10.1007/s11481-025-10271-w","url":null,"abstract":"<p><p>Repetitive traumatic brain injury (RTBI) refers to brain injuries resulting from an external mechanical force causing cumulative and frequently severe neurological consequences. This study aimed to explore the neuroprotective effect of alogliptin (ALO) on RTBI-provoked endoplasmic reticulum (ER) stress and investigate the potential underlying mechanisms. For RTBI induction, rats were exposed to a sharp-edged weight at the right interior frontal area of the right cortex, one drop per day for five successive days. ALO (20 mg/kg/day, p.o.) was administered for one week. Results depicted that ALO recovered motor abnormalities and enhanced motor coordination in the open field test, decreased immobility and increased climbing time in the forced swimming test, and corrected histological aberrations. Moreover, ALO counteracted RTBI-triggered ER stress via suppression of activating transcription factor 6 (ATF6), glucose-regulated protein 78 (GRP78), aggregation of β-amyloid and Tau proteins, as well as elevation of the cortical content of brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrKB). ALO also exhibited an antioxidant and anti-inflammatory potential in addition to its effect on the gene expression of miRNAs (miRNA-322 and miRNA-125b). In conclusion, ALO exhibited a neuroprotective effect by mitigating ER stress induced in an RTBI rat model.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"6"},"PeriodicalIF":3.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12799724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145960749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dexmedetomidine Mitigates Sevoflurane-Induced Neurodevelopmental Effects in Paediatric Anaesthesia: A Meta-Analysis and Preclinical Study. 右美托咪定减轻小儿麻醉中七氟醚诱导的神经发育影响:荟萃分析和临床前研究。
IF 3.5
Hsuan-Chih Lao, Chia-Wei Huang, Ssu-Han Wang, Yen-Lin Su, Chien-Hui Chang, Cheng-Yen Liao, Jen-Chieh Wu, Ying-Chun Lin, Jin-Wu Tsai
{"title":"Dexmedetomidine Mitigates Sevoflurane-Induced Neurodevelopmental Effects in Paediatric Anaesthesia: A Meta-Analysis and Preclinical Study.","authors":"Hsuan-Chih Lao, Chia-Wei Huang, Ssu-Han Wang, Yen-Lin Su, Chien-Hui Chang, Cheng-Yen Liao, Jen-Chieh Wu, Ying-Chun Lin, Jin-Wu Tsai","doi":"10.1007/s11481-025-10273-8","DOIUrl":"10.1007/s11481-025-10273-8","url":null,"abstract":"<p><p>Sevoflurane (Sevo) anaesthesia in children is linked to an increased incidence of postoperative emergence agitation (EA) and potential neurotoxicity in developing brains. However, the specific risks of subanaesthetic foetal or neonatal exposure to Sevo remain unclear. This study evaluates the safety and efficacy of combining dexmedetomidine (Dex) with Sevo to manage EA in paediatric anaesthesia. A systematic review and meta-analysis of randomized controlled clinical trials involving children under 8 years old revealed that Dex significantly reduces EA incidence when administered via intravenous, perineural, and intranasal routes. Using in utero electroporation, we found that pregnant mice exposed to 2.5% Sevo at embryonic days 14.5 and 15.5 exhibited transient neuronal migration deficits, with 25% of neurons delayed in deeper cortical layers. However, these neurons migrated to the cortex by postnatal day 8. Neonatal mice exposed to 2.5% Sevo experienced a 10% reduction in dendritic spine density in adolescence, associated with impaired somatosensory function, as assessed by the Von Frey test. Remarkably, Dex pretreatment ameliorated these pathological and functional changes. Thus, foetal or neonatal Sevo exposure can delay neuronal migration and reduce dendritic spine density. Dex co-administration effectively mitigates these adverse outcomes, supporting its potential use in paediatric anaesthesia to protect developing brains.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"5"},"PeriodicalIF":3.5,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12779744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145914028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gut Microbiome-Sphingolipid Metabolism-Brain Axis Interactions: Neuroprotective Effects of Amitriptyline as Functional Inhibitor of Acid Sphingomyelinase in a Mouse Model of Tauopathy. 肠道微生物群-鞘脂代谢-脑轴相互作用:阿米替林作为酸性鞘磷脂酶功能抑制剂在牛皮病小鼠模型中的神经保护作用。
IF 3.5
Mennatallah Ibrahim, Asmaa M Khalil, Heba Attia, Saleh Alseekh, Ahmed F Mohamed, Mohammed F El-Yamany
{"title":"Gut Microbiome-Sphingolipid Metabolism-Brain Axis Interactions: Neuroprotective Effects of Amitriptyline as Functional Inhibitor of Acid Sphingomyelinase in a Mouse Model of Tauopathy.","authors":"Mennatallah Ibrahim, Asmaa M Khalil, Heba Attia, Saleh Alseekh, Ahmed F Mohamed, Mohammed F El-Yamany","doi":"10.1007/s11481-025-10270-x","DOIUrl":"10.1007/s11481-025-10270-x","url":null,"abstract":"<p><p>Tauopathies are neurodegenerative diseases characterized by accumulation of hyperphosphorylated tau protein (P-tau). The gut microbiota (GM) is symbiotic with the host and altered in neurodegenerative diseases. Amitriptyline (AMI) is a functional inhibitor of acid sphingomyelinase (ASM) which is abnormally highly expressed in brains of Alzheimer patients. Little data is known about the role of colonic ASM in management of tauopathy. Therefore, the aim of this study was to investigate the role of AMI on reversing gut dysbiosis, ceramide levels, colonic inflammation and intestinal barrier disruption in tauopathy through the bidirectional gut-brain axis. P301S transgenic mice were administered AMI for 35 days. Colonic ASM, ceramides, inflammation and membrane integrity were assessed besides fecal microbiome analysis and serum lipopolysaccharides to assess intestinal membrane disruption. Levels of hippocampal P-tau, protein phosphatase 2 A and neurogenesis were assessed along with cognitive behavior. AMI treatment significantly reduced colonic ASM, ceramide levels, increased abundance of Harryflintia, Dubosiella, and Parasutterella and decreased abundance of Lactobacillus, Lachnoclostridium, Oscillibacter, Oscillospiracea UCG-003, Colidextribacter, Roseburia, Butyricicoccus, and Sphingomondales. In contrast, P301S mice displayed an altered GM profile with enriched Firmicutes and Clostridia, and low proportions of Bacteroidota- a phylum associated with intestinal barrier protection-, and Ruminococcaceae. Also, AMI treatment decreased inflammation and restored colonic membrane integrity with subsequent decrease in serum lipopolysaccharides, P-tau in hippocampus and improvement in cognitive behaviour and neurogenesis. The current results indicate that AMI has neuroprotective effects against tauopathy through modulation of ASM activity, associated ceramide levels, GM composition, colonic inflammation and membrane integrity through bidirectional gut-brain axis.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"21 1","pages":"3"},"PeriodicalIF":3.5,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12764700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145897151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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