Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that the Nissl staining images shown in Fig. 3C on p. 427 contained a series of internally duplicated groupings/repeated patternings of cells within the various data panels that could not easily be attributed to coincidence. A subsequent investigation of the data in this paper revealed that the Nissl staining images shown in Fig. 2C were similarly affected by the same phenomenon. After having conducted an internal investigation of the data in this paper, the Editor of International Journal of Molecular Medicine has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 39: 423‑429, 2017; DOI: 10.3892/ijmm.2016.2838].

OBJECTIVES:To compare the biomechanical properties of a novel Ti-3Zr-2Sn-3Mo-25Nb β‑titanium alloy and a traditional Ti-6Al-4V titanium alloy pedicle screw-rod fixation system in posterior lumbar interbody fusion (PLIF). METHODS:In vitro mechanical tests were conducted to evaluate the bending, tensile, compressive, and torsional performance of the β-titanium alloy screws, connecting rods, and the assembled screw-rod fixation system. Two PLIF finite element models were constructed to compare the effects of Ti-6Al-4V versus β-titanium screw-rod systems on range of motion (ROM) and stresses in the endplate and implants. RESULTS:In vitro tests showed that the β‑titanium alloy screw exhibited good resistance to bending (455.95±18.66 N) and torsion (9.03±0.20 N·m). The maximum tensile load of the β-titanium rod was 17 647.06±101.89 N, and the β-titanium screw‑rod system showed a maximum compressive load of 417.65±5.09 N and a maximum torque of 25.00±0.70 N·m. Compared with Ti-6Al-4V, the β‑titanium model showed a 2.6%-8.3% increase in ROM, and the peak stresses in the interbody bone graft, cage, and endplate increased by 1.4%-8.5%, 2.2%-9.4%, and 2.2%-10.1%, respectively, whereas the peak stresses at the bone-screw interface and within the screw-rod system decreased by 8.8%-23.7% and 19.0%-33.1%, respectively. CONCLUSIONS:The β‑titanium pedicle screw-rod fixation system exhibits good in vitro mechanical performance to provide stability comparable to the conventional Ti-6Al-4V system while markedly reducing stress concentration within the screw-rod construct, suggesting its great potential for clinical application.

Polyetherketoneketone (PEKK) has attracted interest for load-bearing orthopedic implants due to its favorable elastic modulus and radiolucency; however, its biological inertness and weak interfacial bonding limit its clinical application. Here, we developed a dual-reinforced PEKK composite by incorporating hydroxyapatite (HA) particles and silicon nitride (SN) nanowires to improve its mechanical, tribological, antibacterial, and osteogenic properties. The ternary PEKK/HA/SN composite (PSH) exhibited tensile, compressive, and flexural strengths of 112.23, 241.36, and 201.48 MPa, increased from 23.04, 92.34, and 60.23 MPa for pure PEKK, respectively. Under dry sliding conditions, PSH showed a friction coefficient of 0.34 and a wear rate of 0.69 × 10− 5 mm3/N·m, corresponding to reductions of 30.6

Robot-assisted gait training (RAGT) and transcutaneous spinal cord stimulation (tSCS) are emerging interventions for incomplete spinal cord injury (iSCI). While tSCS modulates spinal excitability, it remains unclear whether its efficacy is enhanced when paired with high-dose robotic stepping compared to conventional physical therapy (CPT). This prospective, double-blind, randomized controlled trial evaluated 20 adults with iSCI (AIS B–D). Participants were randomized to RAGT + tSCS (n = 13) or CPT + tSCS (n = 7). Both groups received 40 sessions over 8 weeks (5 sessions/week), including 20 min of tSCS using identical parameters. Primary outcomes were the Berg Balance Scale (BBS) and Timed Up and Go (TUG). Secondary outcomes included 10-m walk test (10MWT) speed, Walking Index for SCI II (WISCI-II), ASIA motor score, and intramuscular electromyography (iEMG) of lower-limb musculature. Data were analyzed using repeated-measures MANOVA and univariate general linear models (GLM) to test group × time effects across outcomes, with ANCOVA adjustment for baseline BBS to refine precision. A significant multivariate group × time interaction was observed (Pillai’s trace = 0.982, p < 0.001). Univariate models demonstrated significantly greater gains in the RAGT + tSCS group for BBS (F (1,18) = 42.465, p < 0.001), TUG (F (1,18) = 97.500, p < 0.001), WISCI-II (p = 0.009), and ASIA motor score (p < 0.001). At 8 weeks, the RAGT + tSCS group outperformed the CPT + tSCS group in adjusted BBS (mean difference + 7.67; 95

Introduction:Cervical ossification of the posterior longitudinal ligament (C-OPLL) is a common cause of cervical myelopathy. While mechanical and metabolic factors have been implicated in its pathogenesis, the role of systemic inflammation remains unclear. This research aimed to explore the link between inflammation-related biomarkers and C-OPLL and their predictive ability. Methods:A total of 442 patients (211 C-OPLL, 231 controls) were enrolled in this study. We collected demographic data, comorbidities, and preoperative blood parameters. The calculation of Systemic immune-inflammation index (SII) and other inflammatory indices was performed. Independent risk factors were identified through multivariate logistic regression. Subgroup and interaction analyses assessed the combined effect of body mass index (BMI) and SII on C-OPLL. Results:Patients with C-OPLL showed significantly higher BMI and SII levels than controls (all p < 0.05). Multivariate logistic regression analysis indicated that SII (odds ratio [OR]: 1.121; 95% confidence interval [CI]: 1.101-1.210; P < 0.01) and BMI (OR: 1.412; 95% CI: 1.251-1.594; P < 0.01) were independent predictors of C-OPLL. The AUC for SII on the ROC curve was 0.82. The SII demonstrated a sensitivity of 73.0% and a specificity of 80.5% at a cutoff of 464.2, derived from the current dataset using Youden index analysis. Subgroup analyses consistently showed a positive association between SII and C-OPLL, with no significant interactions detected. A significant synergistic effect was observed between obesity and high SII (P = 0.038). Obese patients with high SII had the highest prevalence of C-OPLL (63.1%) and the greatest risk (OR = 6.23, compared with normal-weight individuals with low SII). Both SII and BMI were independently associated with C-OPLL. Conclusion:These findings suggest that metabolic burden and systemic inflammatory activation may be involved in C-OPLL pathogenesis. Inflammation-based measures such as SII could therefore complement risk stratification, though further research is needed.

Directional cues are essential for orienting cells during tissue morphogenesis and repair. In peripheral nerve regeneration, Schwann cells (SCs) align longitudinally in the nerve bridge to guide axonal pathfinding, but the mechanisms are not fully understood. We show here that after nerve injury, activated SCs up-regulate the guidance receptor Plexin-B1, enabling membrane plasticity required for SC polarization and longitudinal alignment along the axons. Aligned axon-SC provides positional cues to orient macrophages and extracellular matrix. Loss of Plexin-B1 disrupts SC morphological transformation, contact inhibition of locomotion between SCs, and axon-SC alignment, leading to SC misorientation, excessive inflammation, and delayed axon regeneration and functional recovery. These findings identify Plexin-B1 as a key orchestrator to orient SCs by regulating both SC-SC and axon-SC interactions during nerve repair. Elucidating the mechanisms of spatial guidance in nerve repair after injury has potential implications for therapeutic strategies to enhance neural regeneration.

BACKGROUND AND OBJECTIVE:The elastic modulus of cage material (cage-E) is a key determinant of fusion outcomes in oblique lateral interbody fusion (OLIF), as it modulates the efficiency of mechanically induced osteogenesis (EMIO). Here, we establish a logarithmic predictive model linking cage-E to EMIO and delineate the underlying biomechanical mechanisms via computational biomechanical analysis. METHODS:A customized mechano-regulation algorithm was applied to finite element models of the L4/5 OLIF construct to simulate the iteration of tissue differentiation and regeneration, which was driven by mechanical stimulation (MechSt). The regenerative bone fraction at the final iteration was defined as EMIO. A total of 23 cage-E values ranging from 0.1 GPa to 110 GPa were evaluated. RESULTS:As cage-E increased from 0.1 GPa to 110 GPa, the OLIF construct stiffness increased from 3.29 to 6.02 N/mm to 4.95-6.13 N/mm across iterations; the stress-shielding MechSt region expanded from 0 to 0.92% to 9.75-53.67%, whereas the stress-growth MechSt region contracted from 100 to 99.08% to 90.25-46.33%. Correspondingly, EMIO declined from 92.05% to 55.44%. Logarithmic regression revealed strong correlations (R²=0.72-0.89) between cage-E and construct stiffness, MechSt distribution, and tissue regeneration. CONCLUSIONS:Reduced cage-E enhances OLIF EMIO via a defined cascade biomechanical mechanism: cage-E logarithmically regulates construct stiffness, with lower cage-E mitigating stress shielding and preserving the osteogenic MechSt domain, in turn promoting osteoblastic differentiation of mesenchymal stem cells and bone regeneration. The established logarithmic model characterizes the cage-E-EMIO relationship and serves as a potential tool for cage-E screening to optimize OLIF fusion outcomes.

There are an estimated 27 million people living with spinal cord injury (SCI) globally; 20–50% develop hospital-acquired pressure injury during acute care, and the lifetime risk reaches 85% for motor-complete injuries. The use of continuous seated pressure monitoring can provide early warning signs of biomechanical deterioration; however, most smart seat technologies utilize fixed-rate sensor arrays, which can drain battery life after only 4-8 hours and are, therefore, not feasible for consumer level deployment. Existing reinforcement learning methodologies employed to schedule sensors to collect data have optimized generic rewards based solely on data freshness and have not incorporated clinical risk modeling into their optimization, achieving energy efficiency at the cost of missing many high-risk pressure events. This study provides an innovative new approach to seated pressure monitoring (referred to as Risk-Aware Adaptive Sensing with Reinforcement Learning, RAAS-RL) that views seated pressure monitoring as a partially observable Markov decision process (POMDP) and includes the utility of a clinical risk weight when evaluating the incentive to detect seated pressures. RAAS-RL was evaluated on simulated environments derived from PhysioNet pressure-mapping data adjusted with SCI biomechanical parameters and the IoT Sensor Gym framework, achieving 62.5% energy savings, a detection-sensitivity loss of only 1.3 percentage points relative to the full-rate baseline, which alone attains the highest sensitivity but at zero energy savings. This evaluation is simulation-based and does not establish a population-specific clinical finding.

Study designA prospective nonrandomized observational cohort study.ObjectiveTo compare the clinical efficacy of arthroscopic-assisted uniportal spinal surgery combined with unilateral laminotomy bilateral decompression (AUSS-ULBD) and minimally invasive transforaminal lumbar interbody fusion (MIS-TLIF) in the treatment of single-segment stable degenerative lumbar spondylolisthesis (DLS).MethodsA total of 168 patients (AUSS-ULBD n = 86, MIS-TLIF n = 82) with single-segment stable DLS were included. The patients were followed up for at least 2 years. The primary outcome was Oswestry disability index (ODI). Other perioperative indicators, clinical, and radiological outcomes were also compared.ResultsFor ODI, the adjusted mean differences (AUSS-ULBD minus MIS-TLIF) were 1.20 (95% CI -0.85 to 3.25) at 3 months, -1.74 (-3.65 to 0.17) at 12 months, and -0.68 (-2.79 to 1.43) at 24 months. The excellent and good rates of efficacy for the AUSS-ULBD and MIS-TLIF groups were 90.7% and 93.9%, respectively. AUSS-ULBD group had a higher reoperation rate than MIS-TLIF group (difference 4.7%, 95% CI -2.7% to 11.4%, P > .05). The operation time, blood loss, incision length, and hospital stay in the AUSS-ULBD group were lower than those in the MIS-TLIF group (P < .001). At 24 months, lumbar lordosis and slippage improved significantly after MIS-TLIF (P < .05), but not after AUSS-ULBD (P > .05).ConclusionsIn single-level, stable DLS, AUSS-ULBD offered advantages in operative morbidity, while achieving 2-year improvements in pain and disability that were comparable to those of MIS-TLIF. By contrast, MIS-TLIF showed better radiographic correction and lower reoperation rate that did not reach statistical significance.

Propriospinal detour pathways facilitate motor recovery after spinal cord injury (SCI). Here, through a screen of epigenetic modulators, we demonstrated that small interfering RNA (siRNA)-mediated knockdown of histone deacetylase 3, delivered by extracellular vesicles (EVsiHDAC3), promoted neurite outgrowth in murine spinal neurons and human induced pluripotent stem cell-derived sensory and motor neurons. To enhance in vivo efficacy, we developed a neurotrophic nanoparticle platform using gelatin methacryloyl microspheres conjugated with an optimized rabies glycoprotein-derived peptide. Spinal delivery of the EVsiHDAC3-loaded platform (oGHDAC3) or adeno-associated virus-mediated neuronal HDAC3 deletion facilitated propriospino-lumbar detour circuit formation and improved locomotion after staggered double hemisection SCI in mice. Chemogenetic silencing of propriospinal relay neurons compromised recovered stepping upon oGHDAC3 treatment. We observed no therapeutic effects of oGHDAC3 after full spinal transection in mice, further suggesting that spared intraspinal circuits serve as the neural substrates for locomotion recovery. Mechanistically, Stat3 deletion in interlesional neurons, combined with mTOR inactivation, abolished the beneficial effects of oGHDAC3. Finally, combining oGHDAC3 with CLP290, a KCC2 agonist, further improved detour circuit functionality, resulting in consistent weight-supported stepping. Our findings suggest that integrating siRNA-mediated HDAC3 inhibition with a neurotropic bionanomaterial platform could be a translatable approach for restoring motor function after incomplete SCI.

BACKGROUND:Steroid-induced osteonecrosis of the femoral head (SONFH) is a serious bone disease commonly seen in patients on long-term glucocorticoid therapy. Although statins have shown some efficacy in improving lipid metabolism, their efficacy in the treatment of SONFH remains limited. PPARγ inhibitors may enhance the efficacy of statins through several mechanisms. This study aims to investigate how PPARγ inhibitors may enhance the effects of statins in the treatment of SONFH by directly inhibiting apoptosis and indirectly modulating lipoprotein subfractions. METHODS:We first treated osteoblasts in vitro with high concentrations of hormones to simulate the SONFH environment. We then treated the cells with either the PPARγ inhibitor GW9662, the statin lovastatin, or a combination of both. We assessed cell proliferation and apoptosis using CCK-8, flow cytometry and Western blotting. We then established a SONFH rabbit model using high doses of methylprednisolone and lipopolysaccharide. The rabbits were randomly divided into four groups: control group, lovastatin group, GW9662 group and combination therapy group. We observed hip joint MRI before treatment, after 4 weeks of treatment, and 4 weeks after stopping treatment. We performed hematoxylin-eosin staining of the femoral head and analysed serum lipoprotein subfractions using VAP technology. In addition, we used quantitative polymerase chain reaction (qPCR) to analyse the expression of genes related to lipid metabolism at week 3. RESULTS:In vitro experiments showed that both GW9662 and lovastatin effectively inhibited hormone-induced apoptosis. In the animal studies, imaging and pathological results showed that the progression of SONFH was slower in the combination therapy group than in the other groups. VAP analysis showed that the lovastatin group had disturbed lipoprotein subfractions at the fourth week after stopping treatment, while the combination therapy group had more stable lipoprotein subfractions. CONCLUSION:PPARγ inhibitors significantly enhance the efficacy of statins in the treatment of SONFH by directly inhibiting apoptosis and indirectly modulating lipoprotein subfractions. These findings provide new insights into the clinical management of SONFH and suggest that combination therapy may be an effective strategy.

OBJECTIVE:The Cartesian Optoelectronic Dynamic Anthropometer (CODA) motion analysis system is a new instrument that measures 3-dimensional joint movement. The study aimed to investigate the reliability and validity of the CODA motion analysis system in assessing the cervical range of motion in healthy people. METHODS:A total of 41 healthy participants were included. Movements in 3 planes (flexion and extension, right and left lateral bending, and right and left axial rotation) were measured by using the CODA motion analysis system. The results for flexion-extension and lateral bending movements were compared with those obtained by a standard inclinometer. Intraobserver and interobserver reliability and validity were assessed using the intraclass correlation coefficient (ICC) method. SE of measurement (SEM) and minimal detectable change (MDC) values were also calculated to identify the measurement errors. RESULTS:High interobserver reliability (ICC range, 0.89-0.94) and validity (ICC range, 0.73-0.89) were found for all 3 planes, while the intraobserver reliability (ICC range, 0.76-0.92) was high, except for right lateral bending (ICC, 0.76) and left axial rotation movements (ICC, 0.84). All SEM and MDC values for intraobserver, interobserver, and criterion validity studies were less than 5° and 10°, respectively. Percentage of SEM of ≤10% and percentage of MDC of ≤30% were obtained for all variables. CONCLUSION:The CODA motion analysis system is a highly reliable, noninvasive, easy-to-use, and reproducible 3-dimensional device for measuring cervical range of motion. It demonstrated good reliability for flexion-extension and lateral bending movements.

Intervertebral disc degeneration (IDD) is a prevalent condition contributing to back pain and disability. Leukemia inhibitory factor (LIF) has emerged as a protective gene in IDD, prompting further investigation into its role and mechanisms. This study employs bioinformatics analysis combined with experimental validation to explore the role of LIF in IDD. Gene expression datasets from the GEO database were analyzed to identify genes associated with IDD, and the effects of LIF on nucleus pulposus (NP) cell NLRP3 activation and pyroptosis were assessed both in vitro and in vivo. Elevated L IF expression was observed in mildly degenerated discs and decreased in severely degenerated discs. In vitro studies demonstrated that L IF can alleviate IL-1 β-mediated pyroptosis of NP cells and NLRP3 activation by regulating ICAM1 expression. This process is achieved by inhibiting the NF- κB and JAK2/STAT3 pathways. Furthermore, in vivo studies confirmed these findings, showing that the progression of IDD can be ameliorated by expressing LIF or inhibiting ICAM1. LIF and ICAM 1 play significant roles in the pathogenesis of IDD, closely linked to NP cell pyroptosis and NLRP3 activation. Targeting LIF or ICAM1 could offer a novel therapeutic strategy for IDD.

Olfactory ensheathing cells (OECs) are among the most promising cell types for the treatment of spinal cord injury (SCI) and other neural traumas. However, primary OECs cultured in vitro are constrained by their inherent “Hayflick limit,” resulting in poor proliferative and passaging capacities, which restricts their large-scale application in both basic and clinical research. Conditional immortalization technology provides an excellent solution for rapid, large-scale, and controllable proliferation of primary OECs. However, few studies have applied this approach to the controlled passaging of OECs. Here, we used the tetracycline-controlled system (Tet-On system) to introduce the HBLV-TetOn-SV40Tag-PURO constructed into the primary OECs via lentiviral transfection, establishing a conditionally immortalized OEC line. We comprehensively investigated its functional characteristics with or without tetracycline conditions by using immunofluorescence, qPCR, CCK-8, Scratch assay, and Transwell migration experiment. Our results demonstrated that this cell line could rapidly proliferate under tetracycline and quickly recover to proliferation and migration levels similar to primary OECs after tetracycline removal following multiple passages. This approach ensures obtaining a suitable quantity of OECs with specific functional characteristics while avoiding the malignant proliferation risks associated with traditional cell line establishment, thus offering higher safety. Moreover, the method is simple to operate, cost-effective, possessing excellent potential for basic and clinical translational applications.

ABSTRACT Background Lumbar disc herniation (LDH) is a common degenerative spinal disorder that severely impacts patients' quality of life. This study investigated the prognostic values of the lncRNA LINC00638 in LDH and its regulatory role in the senescence of human nucleus pulposus cells (hNPCs). Methods Serum was collected from 93 LDH patients and 108 healthy individuals (matched age and gender). RT‐qPCR was used to detect LINC00638 and miR‐185‐5p expression. The diagnostic and prognostic significance was analyzed using ROC and logistic regression. The hNPCs senescence model induced by 50 ng/mL TNF‐α was established to explore the effects of LINC00638 overexpression (alone or combined with miR‐185‐5p) on cell proliferation, apoptosis, senescence, inflammation, and oxidative stress. Results Serum LINC00638 levels in LDH patients gradually decreased with disease progression (p < 0.05) and were significantly correlated with VAS, JOA and ODI scores (p < 0.001). Low LINC00638 expression was identified as a reliable diagnostic indicator for LDH (AUC = 0.828, sensitivity 70.97%, specificity 80.56%, p < 0.001) and an independent risk factor for poor prognosis (OR = 0.176, p = 0.009). Cellular experiments showed that LINC00638 overexpression significantly inhibited TNF‐α‐induced cell senescence (p < 0.01), while this inhibitory effect was reversed by miR‐185‐5p overexpression (p < 0.05). Conclusions Serum LINC00638 holds promise as a potential biomarker for the diagnosis and prognostic evaluation of LDH, closely reflecting disease severity. Furthermore, LINC00638 participates in regulating hNPCs' senescence and LDH progression by modulating miR‐185‐5p.

Spinal cord injury (SCI) is a highly disabling condition. Olfactory ensheathing cells (OECs) are important transplantable cells for treating spinal cord injury (SCI). However, directly transplanting cells into the injured area may result in the loss of transplanted cells. Additionally, secondary inflammatory responses reduce the survival of transplanted cells. In this study, a hydrogel with favorable properties, including plasticity, strong adhesion, mechanical stability, shear-thinning behavior, and pore size suitable for OEC growth and axon extension, was fabricated from methacryloylated gelatin-pluronic F127 diacrylate (GelMA-F127DA or GEF). In vitro results showed that the GEF hydrogel possessed excellent biocompatibility. Importantly, animal experiments confirmed that transplantation of OECs embedded in the GEF hydrogel effectively repaired SCI, promoted neuronal regeneration and axon remyelination, and improved locomotor function. Accordingly, this treatment strategy offers a new perspective for SCI repair.

Ti6Al4V (TC4) widely used in bone implants, has good mechanical properties but unremarkable bone-forming capacity. Tantalum (Ta) features excellent biocompatibility and suitability for osteogenesis, albeit with a significantly higher elastic-modulus. In this study, we combined the strengths of both materials to optimize implant materials. Magnetron sputtering was applied to deposit a Ta coating onto the TC4 surface (Ta-C-TC4). Surface characteristics were assessed via scanning electron microscope (SEM). Cell adhesion was assessed using SEM and cytoskeletal staining, while live/dead staining was used to evaluate cell viability and biocompatibility on the material surfaces. For proliferation analysis, fluorescence transfection and CCK-8 assay were utilized, while quantification of substance and qRT-PCR were employed to assess the osteogenic differentiation. In vivo, fluorescence labelling, VG, and Goldner staining were employed to evaluate bone integration. A 550 nm-thick Ta coating was successfully achieved on Ta-C-TC4, and its elements and morphology closely resembled Ta. Cells exhibited more pronounced proliferation and differentiation on Ta and Ta-C-TC4. More extensive encasement of new bone was observed around Ta and Ta-C-TC4. Ta-C-TC4 exhibits biocompatibility on par with Ta and demonstrates superior bone integration compared to TC4. Magnetron sputtering represents a promising strategy to harness the mechanical attributes of TC4 with the biological characteristics of Ta, thereby holding potential for the advancement of bone implant.

Intervertebral disc degeneration (IVDD) is a primary contributor to chronic low back pain, affecting over 500 million people globally. In this study, we engineered an injectable collagen-hyaluronic acid (Col-HA) hydrogel incorporating a β-cyclodextrin-resveratrol (β-CD-RES) supramolecular complex, designed to exhibit inflammation-sensitive drug release and promote nucleus pulposus (NP) regeneration. The hydrogel exhibited rapid gelation (within ∼3 min at 37 °C), high compressive strength (35 kPa), and an extended water retention time of 7 h. Drug release analysis showed a sustained resveratrol release, with 60 % released from β-CD-RES and 40 % from β-CD-RES/Col-HA over 96 h. In vitro, the hydrogel supported enhanced NPC proliferation, maintained >90 % cell viability, and significantly reduced ROS levels and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), indicating effective inflammation-facilitated drug delivery. In vivo, rats treated with β-CD-RES/Col-HA showed a marked improvement in disc height index (DHI%), as well as higher expression of COL-II and aggrecan mRNA after 8 weeks. These findings demonstrate the hydrogel's dual role as a supportive scaffold and targeted therapeutic platform for minimally invasive intervertebral disc regeneration.

CAAT/Enhancer Binding Protein β (C/EBPβ) is associated with inflammatory responses in neurodegenerative pathologies, particularly in the brain. However, the regulatory role of C/EBPβ in spinal cord injury and its impact on neurological recovery remain unknown. In this study, we observed significant upregulation of C/EBPβ in microglia after spinal cord injury in mice and was associated with neuroinflammation. Knocking down C/EBPβ in the spinal cord attenuated microglia pyroptosis, reduced the production of proinflammatory cytokines, and inhibited neuronal apoptosis. Mechanistically, C/EBPβ promoted the transcription of Fcgr1, which was involved in activating microglia pyroptosis. In both in-vivo and in-vitro experiments, knocking down Cebpb or Fcgr1, or the pyroptosis inhibitor VX765 inhibited neuronal apoptosis and improved neurological recovery in mice. These findings indicate that C/EBPβ functions as a key regulator that participates in the microglia pyroptosis-mediated neuroinflammation by activating Fcgr1 transcription.