BACKGROUND:Choline kinase alpha is a key enzyme in phospholipid metabolism,involved in the synthesis of phosphatidylcholine,and plays an important role in maintaining cell membrane integrity and signal transduction.Research has shown that choline kinase alpha is highly expressed in various tumors and is closely related to cell proliferation,metabolic reprogramming,and tumor progression.As a potential therapeutic target,the role of choline kinase alpha in tumor metabolism and mitochondrial function still needs further exploration.OBJECTIVE:To evaluate the effects and the underlying mechanisms of choline kinase alpha on the proliferation and apoptosis of glioma U87MG and U251 cells.METHODS:Short hairpin RNA of choline kinase alpha and its empty vector control were transfected into U87MG and U251 glioma cells.Mitochondrial morphology was observed by transmission electron microscopy.Mitochondrial structure and functional protein levels were assessed by western blot assay.Reactive oxygen species levels in cells were measured using a reactive oxygen species fluorescent probe.Mitochondrial membrane potential was assessed with a JC-1 assay.Intracellular adenosine triphosphate levels were measured by chemiluminescence.Cell proliferation was evaluated using a CCK-8 assay.Apoptosis levels were analyzed by flow cytometry.The mitochondrial fission inhibitor Mdivi-1 was used to protect the mitochondrial function of the choline kinase α-silenced lentiviral cells.Finally,U87MG cells were subcutaneously injected to construct a subcutaneous tumor model in nude mice.The tumor growth in nude mice was observed before and after choline kinase alpha silencing and after the use of the mitochondrial fission inhibitor Mdivi-1.RESULTS AND CONCLUSION:(1)Compared with the empty control group,the mitochondria of U87MG and U251 cells in the choline kinase alpha silencing lentivirus group exhibited significant structural abnormalities in mitochondria,such as vacuolization and cristae disruption.The expressions of mitochondrial structure and function-related proteins TOM20,ACO2,and ATP5A were significantly decreased(P＜0.01,P＜0.001),the expression of SOD2 was significantly increased(P＜0.01,P＜0.000 1),the fluorescence intensity of reactive oxygen species was significantly increased(P＜0.01),the mitochondrial membrane potential and adenosine triphosphate level were significantly decreased(P＜0.01,P＜0.001),the cell proliferation ability was reduced(P＜0.01),and the apoptosis level was increased(P＜0.001).(2)Following Mdivi-1 treatment,the fluorescence intensity of reactive oxygen species in U87MG and U251 cells decreased(P＜0.05,P＜0.01),mitochondrial membrane potential and adenosine triphosphate levels were significantly restored(P＜0.05,P＜0.01,P＜0.001),cell proliferation ability was improved(P＜0.05,P＜0.01),and apoptosis level was decreased(P＜0.05).(3)In addition,the in vitro subcutaneous tumor formation experiment of nude mice showed that compared with the empty control group,the mass and growth rate of subcutaneous tumors formed by U87MG cells in the choline kinase alpha silencing lentivirus group were significantly reduced(P＜0.000 1).After Mdivi-1 treatment,the mass and growth rate of tumors were significantly increased(P＜0.000 1).(4)The results show that choline kinase alpha silencing affects the proliferation and apoptosis of glioma cells by inducing mitochondrial dysfunction.

BACKGROUND:Patellar tendonitis can present as tendon degeneration that fails to heal due to tissue overload and incomplete recovery.Patellar tendonitis is a predisposition to high jumping and its pathogenesis has not been clearly defined.OBJECTIVE:To explore the stress-strain relationship of patellar tendon in the take-off technique of high jump through the finite element model with accurate human anatomical structure,so as to provide ideas for the prevention and rehabilitation of patellar tendinitis.METHODS:Based on the CT and MRI imaging data of the lower extremity(including the knee and ankle)of one subject(22 years old,183 cm height,70 kg body mass),a three-dimensional finite element model of the lower extremity was reconstructed using medical imaging software,reverse engineering software and modeling software.The plantar pressure of the take-off leg was collected in eight subjects by gait testing system,and the technical action of high jump take-off was collected by motion capture system.The captured data were imported into human sports biomechanics software for analysis,and kinematic and kinetic data were obtained as the boundary conditions of finite element model for finite element simulation analysis.RESULTS AND CONCLUSION:The force borne by the patellar tendon reached 3.29 times of its own body mass when the subjects took off.In the take-off stage,the peak values of normal equivalent stress,strain and shear stress of the patellar tendon were 127.76 MPa,0.81 and 37.69 MPa,respectively,which were in the nonlinear region of the stress-strain curve,and the peak values were distributed in the proximal and posterior parts of patellar tendon.To conclude,the high patellar tendon force,strain and shear stress caused by the load of 3.29 times its own body mass during take-off are related to the induction of patellar tendinitis.

BACKGROUND:Abutment screw loosening is one of the most common mechanical complications in implant restoration.Mechanical wear,as a potential cause of thread loosening,warrants attention due to its impact on mechanical performance and long-term stability.However,studies on the mechanical effects of thread wear in abutment screws remain limited,and no definitive conclusions have been reached.OBJECTIVE:To investigate the effect of different degrees of mechanical wear on the spatial stress distribution of the Morse taper connection implant system,with a view to providing a theoretical basis for the clinical assessment of the long-term stability of dental implants.METHODS:Three-dimensional finite element models of Morse taper implants with central screw thread wear levels of 0,0.1,1,10,and 100 μm were established using SolidWorks software,and simulation analysis with Ansys Workbench software was performed.The implant models were inserted into artificial bone blocks(simulating type Ⅱ bone,with a cortical bone thickness of 2 mm on the outer layer and cancellous bone inside).An alternating load of 300 N in the buccolingual direction was applied at the centroid of the abutment(forming an angle of 30° with the long axis of the implant).The von Mises stress,principal stress,displacement,and fatigue life of the abutment,central screw,implant,and bone tissue in the five groups of models were analyzed.RESULTS AND CONCLUSION:(1)As the degree of mechanical wear on the central screw thread increased,the von Mises stress,principal stress,and strain in the implant and abutment also increased.The stress in the model was concentrated at the top of the implant,at the shoulder level of the implant,at the neck of the abutment,and at the bottom edge of the abutment.(2)Under moderate wear conditions(≥ 10 μm),the fatigue life of the implant system decreased by 30％,and the maximum von Mises stress of the central screw decreased by 37％,with the stress still primarily concentrated at the transition area between the head and the body of the central screw.(3)Under significant wear conditions(≥ 100 μm),the von Mises stress of the central screw decreased by 98％,with the stress concentrated at the screw head,and the fatigue life of the implant system decreased by 63％.Therefore,when the wear level of the central screw thread reaches ≥ 10 μm,the risk of screw loosening is significantly increased,and the fatigue life of the implant system is markedly reduced,warranting clinical attention.

BACKGROUND:Choline kinase alpha is a key enzyme in phospholipid metabolism,involved in the synthesis of phosphatidylcholine,and plays an important role in maintaining cell membrane integrity and signal transduction.Research has shown that choline kinase alpha is highly expressed in various tumors and is closely related to cell proliferation,metabolic reprogramming,and tumor progression.As a potential therapeutic target,the role of choline kinase alpha in tumor metabolism and mitochondrial function still needs further exploration.OBJECTIVE:To evaluate the effects and the underlying mechanisms of choline kinase alpha on the proliferation and apoptosis of glioma U87MG and U251 cells.METHODS:Short hairpin RNA of choline kinase alpha and its empty vector control were transfected into U87MG and U251 glioma cells.Mitochondrial morphology was observed by transmission electron microscopy.Mitochondrial structure and functional protein levels were assessed by western blot assay.Reactive oxygen species levels in cells were measured using a reactive oxygen species fluorescent probe.Mitochondrial membrane potential was assessed with a JC-1 assay.Intracellular adenosine triphosphate levels were measured by chemiluminescence.Cell proliferation was evaluated using a CCK-8 assay.Apoptosis levels were analyzed by flow cytometry.The mitochondrial fission inhibitor Mdivi-1 was used to protect the mitochondrial function of the choline kinase α-silenced lentiviral cells.Finally,U87MG cells were subcutaneously injected to construct a subcutaneous tumor model in nude mice.The tumor growth in nude mice was observed before and after choline kinase alpha silencing and after the use of the mitochondrial fission inhibitor Mdivi-1.RESULTS AND CONCLUSION:(1)Compared with the empty control group,the mitochondria of U87MG and U251 cells in the choline kinase alpha silencing lentivirus group exhibited significant structural abnormalities in mitochondria,such as vacuolization and cristae disruption.The expressions of mitochondrial structure and function-related proteins TOM20,ACO2,and ATP5A were significantly decreased(P＜0.01,P＜0.001),the expression of SOD2 was significantly increased(P＜0.01,P＜0.000 1),the fluorescence intensity of reactive oxygen species was significantly increased(P＜0.01),the mitochondrial membrane potential and adenosine triphosphate level were significantly decreased(P＜0.01,P＜0.001),the cell proliferation ability was reduced(P＜0.01),and the apoptosis level was increased(P＜0.001).(2)Following Mdivi-1 treatment,the fluorescence intensity of reactive oxygen species in U87MG and U251 cells decreased(P＜0.05,P＜0.01),mitochondrial membrane potential and adenosine triphosphate levels were significantly restored(P＜0.05,P＜0.01,P＜0.001),cell proliferation ability was improved(P＜0.05,P＜0.01),and apoptosis level was decreased(P＜0.05).(3)In addition,the in vitro subcutaneous tumor formation experiment of nude mice showed that compared with the empty control group,the mass and growth rate of subcutaneous tumors formed by U87MG cells in the choline kinase alpha silencing lentivirus group were significantly reduced(P＜0.000 1).After Mdivi-1 treatment,the mass and growth rate of tumors were significantly increased(P＜0.000 1).(4)The results show that choline kinase alpha silencing affects the proliferation and apoptosis of glioma cells by inducing mitochondrial dysfunction.

BACKGROUND:Patellar tendonitis can present as tendon degeneration that fails to heal due to tissue overload and incomplete recovery.Patellar tendonitis is a predisposition to high jumping and its pathogenesis has not been clearly defined.OBJECTIVE:To explore the stress-strain relationship of patellar tendon in the take-off technique of high jump through the finite element model with accurate human anatomical structure,so as to provide ideas for the prevention and rehabilitation of patellar tendinitis.METHODS:Based on the CT and MRI imaging data of the lower extremity(including the knee and ankle)of one subject(22 years old,183 cm height,70 kg body mass),a three-dimensional finite element model of the lower extremity was reconstructed using medical imaging software,reverse engineering software and modeling software.The plantar pressure of the take-off leg was collected in eight subjects by gait testing system,and the technical action of high jump take-off was collected by motion capture system.The captured data were imported into human sports biomechanics software for analysis,and kinematic and kinetic data were obtained as the boundary conditions of finite element model for finite element simulation analysis.RESULTS AND CONCLUSION:The force borne by the patellar tendon reached 3.29 times of its own body mass when the subjects took off.In the take-off stage,the peak values of normal equivalent stress,strain and shear stress of the patellar tendon were 127.76 MPa,0.81 and 37.69 MPa,respectively,which were in the nonlinear region of the stress-strain curve,and the peak values were distributed in the proximal and posterior parts of patellar tendon.To conclude,the high patellar tendon force,strain and shear stress caused by the load of 3.29 times its own body mass during take-off are related to the induction of patellar tendinitis.

BACKGROUND:Abutment screw loosening is one of the most common mechanical complications in implant restoration.Mechanical wear,as a potential cause of thread loosening,warrants attention due to its impact on mechanical performance and long-term stability.However,studies on the mechanical effects of thread wear in abutment screws remain limited,and no definitive conclusions have been reached.OBJECTIVE:To investigate the effect of different degrees of mechanical wear on the spatial stress distribution of the Morse taper connection implant system,with a view to providing a theoretical basis for the clinical assessment of the long-term stability of dental implants.METHODS:Three-dimensional finite element models of Morse taper implants with central screw thread wear levels of 0,0.1,1,10,and 100 μm were established using SolidWorks software,and simulation analysis with Ansys Workbench software was performed.The implant models were inserted into artificial bone blocks(simulating type Ⅱ bone,with a cortical bone thickness of 2 mm on the outer layer and cancellous bone inside).An alternating load of 300 N in the buccolingual direction was applied at the centroid of the abutment(forming an angle of 30° with the long axis of the implant).The von Mises stress,principal stress,displacement,and fatigue life of the abutment,central screw,implant,and bone tissue in the five groups of models were analyzed.RESULTS AND CONCLUSION:(1)As the degree of mechanical wear on the central screw thread increased,the von Mises stress,principal stress,and strain in the implant and abutment also increased.The stress in the model was concentrated at the top of the implant,at the shoulder level of the implant,at the neck of the abutment,and at the bottom edge of the abutment.(2)Under moderate wear conditions(≥ 10 μm),the fatigue life of the implant system decreased by 30％,and the maximum von Mises stress of the central screw decreased by 37％,with the stress still primarily concentrated at the transition area between the head and the body of the central screw.(3)Under significant wear conditions(≥ 100 μm),the von Mises stress of the central screw decreased by 98％,with the stress concentrated at the screw head,and the fatigue life of the implant system decreased by 63％.Therefore,when the wear level of the central screw thread reaches ≥ 10 μm,the risk of screw loosening is significantly increased,and the fatigue life of the implant system is markedly reduced,warranting clinical attention.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveTo clarify whether METTL14 mediates the core role of acupuncture at Neiguan (PC6) in promoting myelination and improving behavior in young autistic rats through gene intervention technology. MethodsThe ASD model was established by intraperitoneal injection of valproic acid (VPA) in pregnant rats. Male offspring were intracerebroventricularly injected with adenovirus-packaged METTL14 shRNA (sh-METTL14) or its control (sh-NC) on postnatal day 1, with a model group set as well. Subsequently, the juvenile rats were divided into model group, acupuncture group, acupuncture+sh-NC group, and acupuncture+sh-METTL14 group. The acupuncture group received acupuncture at Neiguan (PC6) from postnatal day 7, once daily for 21 consecutive days. Neurobehavioral changes were evaluated by behavioral tests; METTL14 knockdown efficiency and the expression of METTL14, METTL3, and PTEN were detected by quantitative real-time PCR (qRT-PCR) and Western blot (WB); PTEN m⁶A levels were measured by RNA immunoprecipitation-qPCR (RIP-qPCR); myelin ultrastructure, expression of myelin basic protein (MBP) and neurofascin 155 (NF155), and dendritic spine density were observed using transmission electron microscopy (TEM), enzyme-linked immunosorbent assay (ELISA), immunofluorescence, qRT-PCR, and primary neuron culture. ResultsBehaviorally, knockdown of METTL14 significantly counteracted the beneficial effects of acupuncture in improving self-grooming, open field exploration, three-chamber social interaction, and Morris water maze learning and memory (P<0.05, P<0.01). Compared with the acupuncture+sh-NC group, the acupuncture+sh-METTL14 group showed significantly decreased mRNA and protein expression of hippocampal METTL14 (P<0.01), and the upregulating effects of acupuncture on METTL3 and PTEN expression were reversed (P<0.01). Meanwhile, knockdown of METTL14 significantly inhibited the acupuncture-induced increase in PTEN m⁶A levels (P<0.01). Morphologically, knockdown of METTL14 attenuated the improvement of myelin structure by acupuncture, reversed the downregulation of MBP and upregulation of NF155 induced by acupuncture, and blocked the increase in dendritic spine density (P<0.05, P<0.01). ConclusionMETTL14 is a key molecule mediating the therapeutic effect of acupuncture at Neiguan. Acupuncture at Neiguan upregulates METTL14, thereby enhancing m⁶A methylation modification of PTEN mRNA to stabilize its expression, ultimately promoting myelin development and improving behavioral symptoms in ASD juvenile rats. This preliminarily reveals the modern biological connotation of “opening Xuanfu and dredging myelin”.

The initiation of adaptive immune responses relies on the precise recognition and interpretation of antigenic information. In this process, the specific binding of T cell receptors (TCRs) to peptide-major histocompatibility complex (pMHC) molecules represents one of the key molecular events in the initiation of adaptive immune responses. Accordingly, the structural features of TCR-pMHC complexes provide a fundamental basis for dissecting antigen recognition mechanisms and support rational vaccine design, therapeutic target discovery in TCR-based immunotherapy, and TCR identification and optimization. However, experimental determination of TCR-pMHC structures remains costly, time-consuming, and limited in coverage, making computational approaches essential for rapidly obtaining reliable structural information. Computational methods for predicting the structures of TCR-pMHC complexes have advanced rapidly in recent years, driven by progress in deep learning-based modeling frameworks and the increasing availability of structural and sequence resources. Despite these developments, most existing tools do not adequately distinguish the key structural and biophysical differences between MHC class I (MHC-I) and MHC class II (MHC-II) complexes during model construction. As a consequence, their predictive performance differs substantially between class I and class II complexes. In general, structural predictions for class I complexes outperform those for class II complexes. This discrepancy may be related to several fundamental differences between the two systems, including the architecture of the peptide-binding groove, the distribution of peptide lengths, and the properties of peptide flanking residues (PFRs). Compared with MHC-I molecules, MHC-II molecules usually bind longer antigenic peptides, which typically range from 13 to 25 amino acids in length. PFRs at both termini of these peptides participate in regulating the overall conformation of TCR-pMHC class II complexes and exert a pronounced effect on the geometric and physicochemical characteristics of the TCR-pMHC binding interface. Furthermore, within the TCR recognition interface, the complementarity-determining regions (CDRs) consist of segments that differ markedly in conformational behavior. They commonly include regions that are relatively rigid and structurally stable, together with highly flexible segments exhibiting substantial conformational plasticity. These rigidity-flexibility features constitute an essential structural basis enabling TCRs to recognize diverse peptide-MHC ligands and to accommodate conformational heterogeneity at the interface. However, many current modeling tools, in an effort to enforce global conformational stability or reduce structural noise, tend to over-constrain intrinsically flexible regions. Such oversimplification may lead to inappropriate rigidification of flexible CDR loops, resulting in local structural distortions, compromised interface geometry, or even complete modeling failure for specific complexes. Against this background, the review approaches the field from the perspective of computational differences between MHC-I and MHC-II complexes. We first systematically organize and summarize available resources related to TCRs and pMHCs, including structural datasets, sequence databases, prediction tools, and benchmarking studies. We then focus on five representative tools capable of predicting both class I and class II complexes—AlphaFold2, AlphaFold3, TCRmodel2, tFold-TCR, and TCR-pHLA_ModellerS. After excluding structures present in the training sets of these tools, we constructed a benchmark dataset comprising 25 class I and 10 class II TCR-pMHC complexes in the bound state and conducted a systematic evaluation using this dataset. We first employ widely used general evaluation metrics, including All-Atom Root Mean Square Deviation (All-Atom RMSD), Backbone RMSD, Template Modeling score (TM-score), and DockQ, to assess the global conformational accuracy and interface modeling quality of class I and class II complexes. For class II complexes, we propose for the first time a peptide flanking residue deviation index, including the PFRs-Deviation Index (PFRs-DI), N-PFR-Deviation Index (N-PFR-DI), and C-PFR-Deviation Index (C-PFR-DI), to quantitatively characterize conformational deviations in PFRs. In addition, we propose the CDR conformational consistency index (CCC) designed to qualitatively evaluate the ability of prediction tools to capture TCR CDR conformational flexibility. These metrics collectively assess a tool’s ability to model both overall conformation and critical functional regions, thereby addressing the limitations of existing evaluation criteria that overemphasize global structure while inadequately capturing modeling quality in key functional areas. This establishes a unified analytical framework for MHC-I and MHC-II complexes to guide data resource selection, modeling strategy formulation, and evaluation system development. The framework further advances computational modeling and provides crucial support for multi-scale analysis of TCR-pMHC recognition mechanisms and their biological functions.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.