Journal of Neuroimmune Pharmacology神经免疫药理学杂志
Journal of Neuroimmune Pharmacology(英文缩写 J NEUROIMMUNE PHARM),ISSN 1557-1890,eISSN 1557-1904,中文译名:神经免疫药理学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.285 | Q1 |
| 2022 | 6.200 | Q1 |
| 2023 | 5.200 | Q1 |
| 2024 | 3.500 | Q2 |
| 2025 | 6.100 | Q1 |
Journal of Neuroimmune Pharmacology 最新收录文献
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1. Pharmacological Profiling of Mefenamic Acid Derivative (2-((2,3-dimethylphenyl)amino)phenyl)(4-ethylpiperazin-1-yl)methone) for its Antidepressant- and Anxiolytic-like Potential Using Corticosterone Induced Depression Model in Rodents.
PMID:期刊:日期:2026-09-19Recent studies demonstrated that serotonergic system, specially 5-HT receptor (5-HTR) plays major role in regulating mood and anxiety. The present study investigates antidepressant- and anxiolytic-like effects of a 5-HT receptor antagonist (5-HTRA), (2-((2,3-dimethylphenyl)amino)phenyl)(4- ethylpiperazin-1-yl)methone) (MP-02), in mouse model of corticosterone-induced depression. Chronic administration of corticosterone (CORT) was done to induce depression- and anxiety-like behaviour in mice. It mimics stress-related pathophysiology due to involvement of HPA axis. Behavioural evaluations, such as spontaneous locomotor activity (SLA), forced swim test (FST), tail suspension test (TST), open field test (OFT), elevated plus maze (EPM), light and dark (L&D) test, sucrose preference test (SPT), were performed to assess antidepressant-and anxiolytic-like effects. Biochemical evaluations such as plasma CORT and serotonin, brain inflammatory marker and oxidative stress marker levels were measured in mouse brain. Administration of MP-02 led to significant reduction in immobility time during the FST and TST and increased % sucrose preference in SPT, which reflects antidepressant-like effect and it enhances the exploratory behaviour in OFT, EPM and L&D test which indicates anxiolytic-like effects. It also decreases the levels of plasma CORT and brain inflammatory markers TNF-α, IL-1β and oxidative stress marker, MDA and increases the levels of brain serotonin and anti-oxidant enzyme catalase and SOD. However, MP-02 was not affected the levels of BDNF in mouse brain. The present study demonstrated the potential antidepressant and anxiolytic-like effects of MP-02 in mice. The results were further supported by docking simulations, offering molecular insights into the understanding of the experimental results.
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2. Sacral Nerve Modulation Alleviates Neuropathic Pelvic Pain Through Modulation of the Spinal Immune Microenvironment and Microglial Activation.
PMID:期刊:日期:2026-09-16To investigate the efficacy of sacral neuromodulation (SNM) in alleviating neuropathic pelvic pain (NPP) and its underlying neuroimmune mechanisms, focusing on microglial activation and the CX3CL1-CX3CR1 pathway. A rat model of NPP was established via pelvic nerve crush (PNC), followed by SNM intervention. Pain behaviors were assessed using von Frey filaments and thermal withdrawal latency testing. Microglial activation, inflammatory factor expression, and signaling pathway dynamics in the spinal dorsal horn were analyzed using immunofluorescence, Western blot, qRT-PCR, and ELISA. Transcriptome sequencing was used to identify key pathways modulated by SNM. Exogenous CX3CL1, LPS, minocycline, and PLX5622 were employed to validate the roles of microglia and the CX3CL1-CX3CR1 axis in SNM-induced analgesia. PNC rats exhibited stable lower abdominal mechanical hypersensitivity, accompanied by significant microglial activation and increased expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the spinal dorsal horn. SNM treatment ameliorated pain behaviors, suppressed microglial activation, reduced pro-inflammatory cytokine expression, and inhibited p38 and p65 phosphorylation. Transcriptome analysis revealed that SNM remodeled inflammation-related transcriptional profiles, notably suppressing the CX3CL1-CX3CR1 signaling axis. Exogenous CX3CL1 or LPS partially reversed SNM-induced analgesia and anti-inflammatory effects. Microglial depletion attenuated the PNC-induced pain phenotype, with no significant synergistic effect observed when combined with SNM. SNM alleviates NPP by inhibiting CX3CL1-CX3CR1-mediated microglial activation and downstream inflammatory signaling, thereby remodeling the spinal cord immune microenvironment. This study provides new evidence for the central immunological mechanism underlying SNM in treating chronic pelvic pain and suggests the CX3CL1-CX3CR1 axis as a potential target for combined neuromodulation therapy.
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3. ELAVL3 Exacerbates Brain Injury and Cognitive Dysfunction in Mice After Cardiac Arrest by Increasing S100B mRNA Stability to Promote Microglia Activation.
3. ELAVL3通过增加S100B mRNA稳定性促进小胶质细胞激活，从而加重小鼠心脏骤停后的脑损伤和认知功能障碍PMID:期刊:日期:2026-09-12Microglial activation-driven neuroinflammation exacerbates secondary brain injury following cerebral ischemia/reperfusion (I/R). The underlying molecular regulators are not fully elucidated. We investigated the role of the RNA-binding protein ELAVL3 and its target S100B in post-ischemic microglial activation and subsequent neuronal injury. In vitro, BV-2 microglia were subjected to oxygen-glucose deprivation/reperfusion (OGD/R), and their conditioned medium was applied to HT22 neurons. In vivo, a mouse model of cardiac arrest/cardiopulmonary resuscitation (CA/CPR) was utilized. Gene expression was modulated using small interfering RNA (siRNA), plasmids, and lentiviral vectors. The ELAVL3-S100B mRNA interaction was confirmed by RNA immunoprecipitation and luciferase assays. Neuronal injury, neuroinflammation, and cognitive outcomes were evaluated using molecular, histological, and behavioral analyses. OGD/R induced pro-inflammatory activation in microglia, leading to neuronal apoptosis, oxidative stress, and mitochondrial damage. ELAVL3 and S100B were upregulated in activated microglia in vitro and in the hippocampus after CA/CPR. ELAVL3 directly bound the S100B 3'-untranslated region, enhancing its mRNA stability and protein expression. In vitro, ELAVL3 knockdown suppressed S100B, attenuated microglial activation, and protected neurons. In vivo, hippocampal knockdown of either ELAVL3 or S100B reduced neuroinflammation and improved cognitive function after CA/CPR. The neuroprotective effects of ELAVL3 knockdown were rescued by S100B overexpression. Our study identifies the ELAVL3/S100B axis as a key driver of post-ischemic neuroinflammation. ELAVL3 enhances S100B expression post-transcriptionally, promoting microglial-mediated neurotoxicity. Targeting this pathway may offer a potential therapeutic strategy for cerebral ischemic injuries.
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4. Tamoxifen Modulates Spinal Cord Injury Repair Via CCL2/CCR2 Axis and its Mechanisms.
PMID:期刊:日期:2026-09-12Spinal cord injury (SCI) represents a profoundly serious neurological disorder characterized by limited self-repair capabilities and accompanied by secondary inflammatory damage, rendering its treatment a pressing challenge in the field of medical science research. During the acute phase of SCI, the expression levels of C-C motif chemokine ligand 2 (CCL2) and its receptor, chemokine receptor 2 (CCR2), are significantly upregulated. The CCL2/CCR2 axis plays a critical role in regulating microglial activation, inflammatory responses, and apoptotic cascades within the injured spinal cord microenvironment. Emerging evidence suggests that tamoxifen (TAM), a selective estrogen receptor modulator, may exert neuroprotective effects in SCI by pharmacologically inhibiting the activity of the CCL2/CCR2 axis. Targeting this axis through TAM administration represents a promising therapeutic strategy to mitigate post-injury pathological progression and improve outcomes in SCI models. This study aims to address the critical issue of secondary inflammatory damage hindering neural regeneration and repair following SCI. By investigating the regulatory effects of TAM on the CCL2/CCR2 axis and its downstream pathways, we seek to elucidate its molecular mechanisms and provide novel strategies for pharmacological intervention in secondary injuries associated with SCI. Utilizing bioinformatics techniques, we identified differentially expressed genes post-SCI and analyzed signaling pathways related to the CCL2/CCR2 axis. We assessed the expression levels of this axis following SCI and employed behavioral assays, RT-PCR, ELISA, and Western blotting to validate the effects of TAM administration on the CCL2/CCR2 axis, its downstream pathways, and molecular mechanisms in both LPS-induced microglial inflammation models and complete transection models of SCI. Furthermore, we utilized the CCR2 antagonist INCB3344 and the PPAR-γ antagonist GW9662 to further validate the relationships within these pathways. TAM significantly reduced the expression of the CCL2/CCR2 axis in both in vitro and in vivo models following injury. By modulating this axis, TAM decreased NF-κB pathway expression and inhibited the secretion of inflammatory factors, facilitating the transition of microglia from a pro-inflammatory to an anti-inflammatory phenotype while activating the PPAR-γ pathway. Additionally, the activation of PPAR-γ reciprocally inhibited the expression of the CCL2/CCR2 axis. TAM may significantly alleviate secondary inflammatory responses following SCI through its modulation of the CCL2/CCR2 signaling pathway, exhibiting anti-apoptotic and anti-inflammatory effects. The findings of this study provide a theoretical foundation and experimental basis for the clinical application of TAM in SCI treatment research.
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5. 6-gingerol Attenuates Inflammatory Response in Rats With Spinal Cord Injury by Reducing NLRP3-mediated Microglial Pyroptosis.
PMID:期刊:日期:2026-08-31Spinal cord injury (SCI) is a severe neurological disorder with limited therapeutic options. 6-gingerol, a major bioactive component of ginger, possesses anti-inflammatory and neuroprotective activities; however, its role in SCI remains incompletely understood. This study investigated the effects and underlying mechanisms of 6-gingerol in SCI-induced microglial pyroptosis. A rat SCI model was established and treated with 6-gingerol. Neurological function, histopathological changes, microglial activation, and pyroptosis were evaluated. An LPS/ATP-induced BV2 microglial pyroptosis model was used for in vitro mechanistic studies. Cell viability, LDH, pyroptosis-related proteins, and inflammatory cytokines were analyzed. The expression of EZH2, USP7, and FOXO3 was determined by qRT-PCR and Western blot. Chromatin immunoprecipitation was performed to evaluate EZH2 and H3K27me3 mediated regulation of the USP7 promoter, while co-immunoprecipitation and ubiquitination assays were used to examine the interaction between USP7 and FOXO3. 6-gingerol significantly improved locomotor recovery, attenuated spinal cord tissue damage, and reduced microglial pyroptosis and inflammatory response after SCI. Mechanistically, 6-gingerol suppressed EZH2 expression and reduced H3K27me3 enrichment at the USP7 promoter, thereby restoring USP7 expression. Increased USP7 enhanced FOXO3 deubiquitination and stabilization, leading to suppression of pyroptotic signaling. Furthermore, EZH2 overexpression, USP7 inhibition, or FOXO3 knockdown partially abolished the anti-pyroptotic effects of 6-gingerol in vitro, and EZH2 overexpression attenuated the neuroprotective effects of 6-gingerol in SCI rats. In conclusion, 6-gingerol treatment alleviates SCI-induced neuroinflammation and microglial pyroptosis through the EZH2/USP7/FOXO3 axis, highlighting a potential therapeutic strategy for SCI.
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6. Palmitic Acid Amplifies Microglial Inflammatory Activation Involving C5aR1-Sensitive Inflammatory Signaling and JMJD3/H3K27me3-Related Epigenetic Changes.
6. 棕榈酸放大微胶质细胞炎症激活，涉及C5aR1敏感性炎症信号传导和JMJD3/H3K27me3相关表观遗传变化PMID:期刊:日期:2026-08-26Microglial pro-inflammatory activation contributes to neuroinflammatory processes in many neurological disorders. Saturated fatty acids such as palmitic acid (PA) are increasingly recognized as inflammatory cues, yet the molecular mechanisms linking PA to microglial inflammatory responses remain incompletely defined. In this study, using BV-2 microglia as an exploratory in vitro model, we investigated whether C5aR1-sensitive signaling and JMJD3/H3K27me3-related epigenetic changes are involved in PA-associated inflammatory responses. PA exposure increased Iba1 expression, altered CD86/CD206 expression, and enhanced the secretion of IL-1β, IL-6 and TNF-α. Exogenous C5a produced broadly similar inflammatory changes. Under heat-inactivated serum conditions, PA increased cell-associated C5a immunoreactivity and extracellular C5a levels, and these C5a-related readouts were reduced by PMX53. PMX53 also attenuated PA-associated increases in inflammatory markers and in the expression of TLR4, total NF-κB p65, c-Fos, and c-Jun. In parallel, PA and C5a increased JMJD3 expression and JMJD3 enrichment at selected IL-1β and IL-6 promoter regions, accompanied by reduced H3K27me3 enrichment at these loci. Pharmacological KDM6 inhibition with GSK-J4 attenuated PA-associated increases in IL-1β and IL-6 expression. Together, these findings support the involvement of C5aR1-sensitive inflammatory signaling and JMJD3/H3K27me3-related epigenetic regulation in PA-associated microglial inflammatory responses.
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7. Altered Pannexin2 Expression in Retinal Degeneration: Insights from the P23H Mouse Model of Retinis Pigmentosa.
PMID:期刊:日期:2026-08-25Pannexins are large channels involved in purinergic signaling within the nervous system. However, their role in human disease and their therapeutic potential remain poorly understood, particularly for Pannexin-2 (Panx2). The aim of this study was to investigate whether Panx2 is associated with retinal neurodegenerative diseases. Using immunohistochemistry and flow cytometry, we analyzed Panx2 expression in the retina of the P23H mouse model of retinitis pigmentosa and in control C57BL/6J mice. We observed that healthy retinas contained a small population of Panx2-positive cells. In contrast, the Panx2 positive population was increased in the retinas of P23H retina, particulary at advanced stages of the disease. Panx2 was found to co-occur with the purinergic receptors P2X7R but not with P2X4R. This result was further supported by the reanalysis of RNA-seq data from GEO functional genomics data repository, which indicated an increased Panx2 mRNA expression in P23H mice at intermediate stages of the disease, compared with control animals. Together, these findings suggest that Panx2 expression is altered during retinal degeneration in the P23H model and may be associated with purinergic signaling pathways involved in disease progression. These results raise interesting questions for further investigation regarding the role of Panx2 in retinal degeneration.
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9. Crosslink Between Neuroinflammation and Oxidative/Nitrosative Status in the Glioblastoma Tumor Microenvironment: Prognostic and Theranostic Impact.
PMID:期刊:日期:2026-08-20Glioblastoma (GB) is the most aggressive primary brain tumor, characterized by rapid progression, therapeutic resistance, and poor prognosis. Increasing evidence suggests that oxidative and nitrosative stress, together with a proinflammatory tumor microenvironment (TME), play a critical role in gliomagenesis. In this study, we analyzed a cohort of 89 Algerian patients with GB glioblastoma, to characterize systemic and intratumoral oxidative/ nitrosative status. Hydrogen peroxide, malondialdehyde, total nitrite levels, and catalase activity were quantified in serum or plasma, cystic fluid, and tumor homogenates to assess redox balance across different histological glioblastoma subtypes. In parallel, tumor expression of proinflammatory cytokines: interleukin-6 (IL-6), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and key mediators of tumor progression: Nuclear factor kappa B p65 (NF-κB p65), inducible nitric oxide synthase (iNOS) and vascular endothelial growth factor (VEGF), was evaluated. Additionally, we investigated the interplay between redox balance and inflammatory signaling, and its potential implications for prognosis and theranostic therapeutic decision-making. Our findings demonstrated systemic and intratumoral redox imbalance in serum/ plasma compared with TME tumor microenvironment compartments, without impact from any subtypes. However, we noted pronounced intratumoral proinflammatory cytokines expression, as well as NF-κB p65, iNOS and VEGF in most cases, consistent with ongoing neuroinflammatory signaling, a highly reactive TME and more aggressive histopathological features. Combined assessment of oxidative/ nitrosative stress biomarkers and proinflammatory cytokines provides valuable insight into GB glioblastoma prognostic relevance. Targeting redox imbalance and inflammatory pathways within the GB glioblastoma TME represents a promising strategy to enhance therapeutic efficacy and improve patient outcomes.
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10. Low-Dose Cannabidiol Treatment does not Alter Cognitive Performance in the HIV-1 Transgenic Rat Model of NeuroHIV.
PMID:期刊:日期:2026-08-20HIV-associated neurocognitive impairment (NCI) remains prevalent among virally suppressed people living with HIV (PLWH) and approved treatments target these symptoms. Cannabidiol (CBD), a non-intoxicating cannabinoid with neuroprotective and anti-inflammatory properties, has been proposed as a potential therapeutic candidate for HIV-associated NCI, yet its cognitive effects in the context of HIV have not been experimentally tested. Female and male HIV-1 transgenic (HIV-1Tg; n = 57) and Fischer 344 (F344; n = 57) control rats were assessed using a translational cognitive battery measuring risk-based decision-making (Iowa Gambling Task; IGT), learning and cognitive flexibility (Probabilistic Reversal Learning Task; PRLT), and effortful motivation (Progressive Ratio Breakpoint Task; PRBT). Animals were tested at baseline to establish innate cognitive performance, then retested following acute and chronic (16-day) CBD administration (0, 0.3, and 3 mg/kg). HIV-1Tg rats exhibited subtle IGT deficits and persistent reversal learning deficits in the PRLT, with preserved learning and motivation, modeling key features of HIV-associated NCI. These selective impairments in cognitive flexibility persisted across testing periods, with performance in other domains largely intact. CBD produced modest, dose-specific effects on response latencies and motivation but did not affect cognitive performance. HIV-1Tg rats exhibited selective cognitive deficits similar to those seen in PLWH, supporting their utility as a preclinical model of HIV-associated NCI. Across multiple translatable cognitive domains CBD did not significantly alter cognitive performance in HIV-1Tg rats at the doses tested. Further research using broader dosing, different administration routes, and co-administration with other cannabinoids is needed to fully explore the therapeutic potential of CBD for targeting HIV-associated NCI.