ObjectiveTo study the mechanism of electroacupuncture （EA） of “Shangjuxu”（ST37） underlying improvement of colonic dysmotility in ulcerative colitis （UC） mice through regulating cyclic nucleotide-gated cation channel 2 （HCN2）.MethodsMale C57BL/6J mice were randomized into control， model and EA groups， with 8 mice in each group. The UC model was established by giving 2.5% Dextran Sulfate Sodium （DSS） to the mice. EA （2 Hz/100 Hz， 0.9 mA） was applied at bilateral ST37 for 20 min， once a day for 7 days. The body weight， stool appearance and bloody stool conditions were recorded and the disease activity index （DAI） score was determined. The morphological changes of the colonic tissue were observed after H.E. staining. The changes of colonic motility before and after EA intervention were assessed by using in vivo and in vitro electrophysiological methods. The colonic transit time （glass bead method） and intestinal propulsion rate （ink mark method） were calculated. The immunofluorescence intensity values of colonic hyperpolarization activated HCN2， 5-hydroxytryptamine （5-HT）， tryptophan hydroxylase 1 （TPH1）， and serotonin transporter （SERT） were detected by immunofluorescence staining. The expression levels of TPH1 and SERT mRNAs and proteins were detected using real-time quantitative PCR and Western blot separately. The Vil1MerCreMer mice were randomly divided into a control group and an induction group， with 8 mice in each group. The Vil1MerCreMer mice were specifically conditionally knocked out of the HCN2 gene in the intestinal epithelium. The mice in the induction group were injected with 5 mg/mL tamoxifen. ELISA was used to detect the contents of 5-HT and cyclic nucleotides （cAMP） in the serum； real-time quantitative PCR was used to detect the expression of HCN2 and TPH1 mRNA in the colon. The RIN-14B cells were divided into a normal group and a transfection group. The transfection group knocked down the expression of HCN2 in the RIN-14B cells. ELISA was used to detect the expression of 5-HT and cAMP in the cell supernatants.ResultsIn contrast to the control group， the model group showed a significant decrease in the body weight and a notable increase in the DAI score and histopathological score （all P<0.001）. In vivo and ex vivo electrophysiology showed that DSS mice had significant colonic motility dysfunction， decreased frequency， amplitude， and the area under the curve （AUC） of colonic pressure curves （all P<0.001）. Colonic transit time was strikingly prolonged while propulsion rate was significantly lower in DSS mice （all P<0.001）. Colonic HCN2， co-localized with 5-HT， was markedly increased in the expression （P<0.001）， along with elevated expression of 5-HT， TPH1 and SERT （all P<0.001）. All the increase and decrease of the indexes mentioned above were reversed by EA （ P<0.001， P<0.01，P<0.05）. Conditional deletion of HCN2 in the intestinal epithelium markedly reduced the serum contents of 5-HT and cAMP （ P<0.001）. Knockdown of HCN2 in RIN-14B cells reduced the expression levels of HCN2 and TPH1 mRNAs （P<0.001）， along with a significant decrease of the contents of 5-HT and cAMP in the cell supernatant （P<0.001）.ConclusionEA at ST37 can improve colonic motility in UC mice by modulating the expression of HCN2 in EC cells and regulating the release of 5-HT.

Acupuncture omics data analysis enables a deep understanding of the physiological mechanisms and therapeutic effects of acupuncture. However, such omics data are often high-dimensional and require non-negativity constraints, posing significant challenges for analysis methods. To address these issues, we propose a deep non-negative matrix factorization algorithm for acupuncture omics data clustering (DNMOC). First, the omics data is transformed into low-dimensional matrices by non-negative matrix factorization (NMF). Second, these low-dimensional matrices elements are non-negatively restricted using an activation function and updated by stochastic gradient descent method. Third, the gradient values corresponding to element updates are transformed into biases and weights, which are combined with the nonlinear function to construct the DNMOC network. Fourth, the DNMOC network is used to realize the learning of the low-dimensional matrices. Finally, extensive experiments on six acupuncture omics datasets demonstrate that our algorithm outperforms contemporary methods.

Primary dysmenorrhea （PD） is a common gynecological disorder affecting women of reproductive age worldwide， characterized by high prevalence， recurrent attacksand impaired quality of life. Acupuncture has definite therapeutic effects on PD， and related studies on its mechanism are increasingly deepening. The core pathogenesis of PD is the disordered brain-body bidirectional interaction. From the perspective of brain-body interaction， this paper systematically summarizes the mechanisms of acupuncture in intervening PD， including synchronously regulating central networks such as default mode network， sensorimotor network， and descending pain modulatory system， modulating signaling pathways including hypothalamic-pituitary-ovarian axis， hypothalamic-pituitary-adrenal axis， Toll-like receptor 4/nuclear factor-κB， and phosphatidylinositol 3‑kinase/protein kinase B/mammalian target of rapamycin， as well as improving uterine local pathological status， optimizing uterine blood flow， correcting prostaglandin imbalance， and relieving smooth muscle spasm. These effects synergistically block the brain-body vicious cycle of PD and achieve multi-system， multi-level holistic regulation and long-lasting analgesia.

Acupuncture is an effective treatment method for diseases and is widely used around the world. However, research on acupuncture prescription recommendations based on symptom sets remains in the exploratory phase. To address this gap, we propose a hybrid pooling heterogeneous graph fusion (HyPoHGF) algorithm. Specifically, we first construct an acupuncture heterogeneous graph (AcuHG) dataset containing 2,325 prescriptions. It includes 464 symptoms, 414 acupoints, and 26 acupoint properties. Then, we employ a frequency-aware graph convolutional network for message aggregation among nodes and utilize subgraph aggregation to learn complex relationships among symptoms, acupoints, and acupoint properties. Next, a hybrid pooling mechanism is used to generate main-adjunct acupoint prediction scores. Finally, extensive experiments on the AcuHG dataset and a public herbal prescription dataset demonstrate that HyPoHGF outperforms state-of-the-art algorithms. This work publishes the first public acupuncture prescription recommendation dataset along with source code, available at: github.com/LONGsci/HyPoHGF.

ObjectiveTo explore the response characteristics of whole-brain c-Fos signals in brain regions associated with acupuncture and moxibustion analgesia， and to identify potential targets for revealing differences in the central regulatory mechanisms underlying their analgesic effects.MethodsC57BL/6J mice were randomly divided into sham， model， acupuncture， and moxibustion groups， with 8 mice in each group. Neuropathic pain was induced by spared nerve injury （SNI） of the sciatic nerve. The acupuncture and moxibustion groups received electroacupuncture and moxibustion interventions respectively for 30 min each day at “Zusanli” （ST36） for 7 consecutive days. Mechanical and thermal pain thresholds were measured to assess analgesic efficacy. Whole-brain c-Fos expression was detected by immunofluorescence. Bioinformatics methods were employed to analyze the number of analgesia-responsive brain regions， shared and specific regions， functional brain networks， and hub nodes based on c-Fos expression levels.ResultsAfter the final treatment， compared with the sham group， the model group showed significantly decreased mechanical and thermal pain thresholds （P<0.001）. Compared with the model group， both acupuncture and moxibustion groups showed significantly increased thresholds （P<0.01， P<0.001）， with the acupuncture group exhibiting significantly higher thresholds than the moxibustion group （P<0.05）. Whole-brain c-Fos signals were significantly increased in the model group compared with the sham group， while both treatment groups showed significant reductions relative to the model group. A total of 48， 6 and 13 brain regions presented significant alterations in c-Fos signals in the SNI group， acupuncture group and moxibustion group， respectively. In the acupuncture group， the significantly altered brain regions mainly included the primary cingulate cortex area 1 （Cg1R，L）， paraventricular nucleus of the hypothalamus （PVNR）， primary somatosensory cortex hindlimb region （S1HLL）， basolateral amygdala （BLAL）， magnocellular part of the paraventricular hypothalamic nucleus （PaLML）， and left posterior paraventricular hypothalamic nucleus （PaPoL） （P<0.05， P<0.01）. For the moxibustion group， the prominent brain regions with changed c-Fos signals were the locus coeruleus （LCR，L）， ateral hypothalamus （LHR，L）， ventral part of the medial geniculate nucleus （MGVL）， right and left paraventricular nucleus of the hypothalamus （PVNR，L）， S1HLL， Cg1R，L， BLAR，L， basomedial amygdala （BMAL）， substantia nigra （SNR）， and mediolateral secondary visual cortex （V2MLR） （P<0.05， P<0.01， P<0.001）. Within the analgesic brain functional networks of acupuncture and moxibustion， the primary somatosensory cortex （S1R）， dorsomedial thalamic nucleus （DenL） and dorsomedial hypothalamic nucleus （DMR） served as common significantly responsive nodes. S1， Dorsal Endopiriform Nucleus （Den） and central amygdala （CeCL） were identified as nodes with strong functional connectivity in both networks. In addition， the cornu ammonis 2 region of the hippocampus （CA2R） and CeC represented the nodes with the highest connectivity degree in the acupuncture network and moxibustion network， respectively.ConclusionAcupuncture shows superior analgesic effects to moxibustion in the SNI model. Both interventions likely exert analgesia primarily through negative activation across multiple brain regions. Cg1， PVN， S1HL， and BLA may be shared response regions； PaPo and PaLM may be specific to acupuncture； and LC， LH， MGV， SN， BMA， and V2ML may be specific to moxibustion. S1， Den， and CeC may represent shared functional network pathways， while CA2 and CeC may serve as core hubs in the acupuncture and moxibustion analgesic brain networks， respectively.

Beyond somatic initiation, cancer progression is governed by a multidimensional systemic metabolic architecture. This permissive macroenvironment, shaped by systemic nutrient fluxes, endocrine networks, and microbial co-metabolites, sustains tumor bioenergetics and immune evasion. Bridging the current translational gap requires decoding the spatiotemporal reciprocity between diet-induced metabolic shifts, tumor microenvironment plasticity, and genotoxic therapy responses. In this review, we deconstruct the host-tumor metabolic interface through a systems biology framework, tracing the biotransformation of macro-dietary inputs into subcellular oncogenic and immunological signals. We move beyond traditional nutritional epidemiology to define a precision nutritional oncology paradigm that leverages high-resolution multi-omic biomarkers to track real-time systemic flux, the spatial ecosystem of the microbiome as a localized metabolic bioreactor, and context-dependent metabolic regulation to exploit transient tumor vulnerabilities. We emphasize the need for precise spatiotemporal calibration, particularly during acute refeeding windows, to prevent paradoxical therapy resistance or accelerated cachexia. Finally, we envision a future in which precision nutrition is seamlessly integrated into oncologic care, powered by artificial intelligence and digital gut twins for in silico modeling. By incorporating the broader chemical exposome and addressing structural socioeconomic determinants through frameworks such as the Planetary Health Diet, we outline a roadmap toward global health equity and enhanced metabolic resilience in cancer survivorship.

This narrative review synthesizes preclinical evidence from 54 studies to outline the distinct, stage-dependent mechanisms of manual acupuncture (MA) and electroacupuncture (EA) in inflammatory pain. Following a systematic search, we conducted a detailed thematic analysis of studies using CFA-induced rodent models and organized the findings into three pathological phases: acute (1-3 days), subacute (4-14 days), and chronic (>14 days). The results demonstrate a temporal evolution of therapeutic mechanisms that underscores the necessity of stage-specific intervention strategies for optimizing clinical outcomes. In the acute phase, interventions primarily produce rapid analgesia by engaging immediate descending inhibitory pathways and modulating peripheral ion channels. During the subacute phase, treatments work to counteract central sensitization through immune microenvironment reprogramming and the regulation of synaptic plasticity. For the chronic phase, strategies expand beyond pain relief to alleviate neuropsychiatric comorbidities and promote systemic tissue repair via limbic circuit remodeling. By integrating these findings, this work proposes a time-sensitive mechanistic framework. It underscores the principle of "time-window" optimization for precision acupuncture intervention in inflammatory pain, while also pointing to the critical need for future clinical translation and validation.

Background:Acupuncture is widely used for chronic non-specific low back pain (CNLBP), yet the optimal dosing parameters remain unclear. This systematic review and meta-analysis evaluated the overall efficacy of acupuncture for CNLBP and explored dose-response relationships between acupuncture parameters and pain reduction. Methods:PubMed, Embase, the Cochrane Library, and Web of Science were searched from inception to December 2025 for randomized controlled trials (RCTs) comparing acupuncture with sham, no-intervention, or active controls. The primary outcome was end-of-treatment pain intensity (VAS/NRS). Effect sizes were expressed as Hedges' g and pooled using a random-effects model (REML, Knapp-Hartung). Dose-response relationships for treatment sessions, duration, and needle retention time were examined by weighted meta-regression with restricted cubic splines (RCS). Results:Twelve randomized controlled trials involving 1,155 participants were included. Acupuncture significantly reduced pain intensity compared with controls (pooled Hedges' g = 0.57, 95% CI: 0.19-0.95), with substantial between-study heterogeneity (I2 = 85.3%). Exploratory dose-response and subgroup analyses indicated a potential nonlinear association for treatment duration - notably with a possible plateau or turning range around 6-7 weeks - though it was sensitive to the most influential trial and must be viewed as hypothesis-generating. Total sessions, needle retention time, and treatment frequency showed no significant dose-response relationships. No publication bias was detected, though statistical power was limited. Conclusion:Acupuncture provides moderate pain relief for CNLBP. The observed nonlinear duration signal-including a potential turning range around 6-7 weeks-is preliminary and hypothesis-generating, given the high heterogeneity and sensitivity to the most influential trial. Session number and needle retention time showed no detectable dose-response association within the available evidence. Dedicated dose-finding trials are required.

Normal physiological brain activity relies on precise and orderly energy supply. The brain’s complex energy metabolism (encompassing glucose, lipid, lactate, and amino acid metabolic pathways) underpins neuronal function. Neuropathic pain severely impacts patients’ quality of life, and traditional therapies often prove ineffective. This condition is frequently accompanied by energy metabolism disorders in relevant brain regions. Dysregulation of metabolic pathways disrupts neuronal energy supply and signaling, impairs synaptic transmission, and triggers abnormal glial interactions and neuroinflammation, thereby driving the onset and chronic progression of neuropathic pain. This paper systematically elucidates the impact of metabolic pathway imbalances on neuropathic pain and explores potential therapeutic strategies targeting energy homeostasis. It aims to provide novel theoretical foundations and treatment approaches for the clinical management of neuropathic pain.

Neurodegenerative diseases (NDs) are progressive disorders characterized by neuronal degeneration in the central nervous system (CNS), ultimately leading to neurological dysfunction. Neurodegenerative progression is often associated with structural and functional alterations in perineuronal nets (PNNs). With the continuous advancement of sequencing technologies and omics disciplines, numerous techniques have been widely applied to studies on PNNs. Research on PNNs is beneficial for understanding the pathogenesis and clinical diagnosis of NDs and finding new drug treatment targets. In this review, we paid attention to these omics technologies used in PNNs and also summarized some alterations in PNNs in NDs.

A sustained imbalance between excitatory and inhibitory mechanisms within the glutamatergic and GABAergic systems of the cerebral cortex, induced by noxious stimuli, is a fundamental characteristic in the development and maintenance of chronic pain. This review provides a comprehensive summary of the roles and interaction of glutamatergic and GABAergic systems in the processing of chronic pain signals. Specifically, we present a systematic summary of the processing patterns of the cerebral cortex in the cross-modular integration and output of chronic pain information, according to four aspects, molecular, cellular, neural network and behavioral cognition. These patterns consist of neuronal responses in individual cortical regions, neuron-astrocyte interactions, sharing and cascading of inter-cortical signals, and downward cortical modulation. Furthermore, a number of potential therapeutic approaches to the chronic pain are discussed from the pain management perspective.

Acupoint sensitization theory guides clinical diagnosis and treatment, positing that disease factors alter the state of acupoints, typically manifesting as changes in temperature, resistance, and pain threshold. Flexible sensors can rapidly detect sensitized acupoints and evaluate efficacy by measuring the resistance and temperature values of acupoints. Consequently, utilizing ultra-thin polyimide as a substrate, the research group developed a flexible sensor capable of simultaneously detecting acupoint temperature and resistance while providing therapeutic functions. the designed sensor features a compact size, low mass, high flexibility, and high measurement accuracy. It achieves a temperature measurement accuracy of 0.002-0.02 degrees C within the range of 0-40 degrees C. The detection error falls within the range of 10.5 to 17.5 Omega within the range of 2.1K Omega to 100K Omega. Furthermore, the designed sensor has been applied to human sensitized acupoint monitoring and intervention experiments, demonstrating favorable performance, which offers potential for future acupoint sensitization research.

Objective:To observe the effect of electroacupuncture (EA) on the intestinal flora in rats with chronic obstructive pulmonary disease (COPD) and explore its possible mechanism based on the gut-lung axis theory. Methods:A total of 30 male SD rats of SPF grade were randomly divided into a normal control (NC) group, a model group and an EA group, 10 rats in each one. In the model group and the EA group, COPD model was established by intratracheal instillation of lipopolysaccharide combined with cigarette fumigation. In the EA group, EA was applied at bilateral "Feishu" (BL13) and "Zusanli" (ST36), with disperse-dense waves, in frequency of 4 Hz/20 Hz, current of 1-3 mA, 20 min a time, once a day for 14 days continuously. Before and after modeling, as well as after intervention, body weight was observed; after intervention, the lung function indexes (forced expiratory volume in 0.1 second [FEV0.1], FEV0.1/forced vital capacity [FVC]%, forced expiratory volume in 0.3 second [FEV0.3] and FEV0.3/FVC%) were measured, serum levels of inflammatory factors (tumor necrosis factor-α[TNF-α], interleukin-6[IL-6], interleukin-1β[IL-1β] and interleukin-10[IL-10]) were detected by ELISA, histopathology of lung and colon tissues was observed by HE staining, the intestinal flora were analyzed by 16S rRNA, and the correlations between lung function and intestinal flora were analyzed. Results:Compared with the NC group, in the COPD group, the body weight and lung function indexes were reduced (P<0.01); the lung and colon tissues were damaged, the mean linear intercept (MLI) of alveolus and inflammatory cell numbers of 100 μm2 in lung tissue were increased (P<0.01); the serum levels of TNF-α, IL-6 and IL-1β were increased (P<0.01, P<0.05), and the serum level of IL-10 was decreased (P<0.01); α-diversity indexes of intestinal flora were increased (P<0.01); the relative abundance of Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus was increased (P<0.01), the relative abundance of Firmicutes, Actinobacteria, Tenericutes, TM7 and Lactobacillus, Allobaculum, Bifidobacterium, YRC22 was decreased (P<0.01, P<0.05); 31 different expressed metabolic pathways were identified between the two groups. Compared with the COPD group, in the EA group, the body weight and lung function indexes were increased (P<0.01); the damage of lung and colon tissues was improved, the MLI of alveolus was decreased (P<0.05); the serum levels of TNF-α, IL-6 and IL-1β were decreased (P<0.05), and the serum level of IL-10 was increased (P<0.05); α-diversity indexes of intestinal flora were decreased (P<0.01); the relative abundance of Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus was decreased (P<0.01, P<0.05), the relative abundance of Firmicutes, Actinobacteria, Tenericutes, TM7 and Lactobacillus, Allobaculum, Bifidobacterium, YRC22 was increased (P<0.01); 35 different expressed metabolic pathways were identified between the two groups. The lung function was positive related with Actinobacteria, Tenericutes, TM7 and YRC22, and was negative related with Bacteroidetes, Proteobacteria and Oscillospira, Bacteroides, Coprococcus. Conclusion:EA may ameliorate lung function and tissue injury of COPD by regulating intestinal flora dysbiosis and inflammatory response, suggesting an anti-inflammatory effect mediated via "gut-lung" axis.

Ulcerative colitis (UC) and Alzheimer's disease (AD) share a common etiology as inflammatory diseases characterized by barrier deterioration. The aim of this study is to elucidate how neutrophil extracellular traps (NETs), serving as a comorbid etiological factor, can trigger the dysfunction in both the intestinal barrier and blood-brain barrier (BBB). Integrated bioinformatics analysis revealed 14 overlapped NETs-related differential expressed genes in UC and AD, which strongly featured barrier dysfunction. The following verification experiments identified enriched NETs, as well as damaged intestinal epithelium and BBB permeability, in the colon and prefrontal cortex of colitis mice and APP/PS1 mice. By employing pharmacological interventions (Cl-amidine and Disulfiram), we disrupted the formation of NETs and discovered significantly restored barrier integrity and attenuated inflammation. Further enrichment and correlation analysis indicated, for the first time, DDIT4/IL-1 beta NETs might drive macrophage-mediated phagocytosis to induce barrier dysfunction in UC and AD. Our findings originally established the peripheral-central inflammation interactions of UC and AD from the perspective of NETs, highlighting the potential valuable roles in gut-brain interactions and future clinic translational therapeutics.

The molecular mechanisms of brain-body interactions in the progression of brain diseases remain unknown. Through integrative analysis of multi-organ proteomic, metabolomic, and transcriptomic data following ischemic stroke, we identified dynamic molecular signatures across organs. The heart exhibited the highest number of differentially expressed proteins (DEPs), followed by spleen and intestine. Ten DEPs were shared among three organs post-stroke, with eight in heart, six in spleen, and five in intestine. Notably, organs displayed accelerated biological aging, particularly the intestine, ‌which is implicated in neurobehavioral regulation. Conjoint analysis further confirmed that DEPs originated from both intrinsic and immune cells that systemically infiltrated multiple organs. Finally, plasma DEPs showed high correlations with corresponding protein levels in distinct organs, potentially resulting in the systemic circulation of stroke. Our findings provide a comprehensive atlas of stroke-induced multi-organ molecular remodeling and establish a foundational framework for developing systemic therapeutic strategies targeting brain-body interactions in brain injury.

Objective:Based on a complete Freund's adjuvant (CFA)-induced chronic inflammatory pain model, we compared and analyzed the differences in anti-inflammatory and analgesic effects of moxibustion intervention initiated at different timepoints, aiming to identify the optimal timing for moxibustion intervention. The goal is to establish standardized intervention protocols for basic research on the anti-inflammatory and analgesic effects of moxibustion. Methods:Male C57BL/6 mice were randomly divided into 3 groups based on the moxibustion initiation timepoints of 4, 7, and 10 d after modeling. Then, the mice in each group were randomly assigned to 3 subgroups, including a control group, a model group, and a moxibustion group, with 8 mice in each subgroup. Chronic inflammatory pain was induced by injecting 20 μL of CFA into the sole of the right hind paw. Moxibustion applied at the "Zusanli" acupoint for 30 minutes started on the 4th, 7th, and 10th days after modeling, and the intervention continued for 7 days. The latency of paw withdrawal to thermal radiation was measured to evaluate the pain threshold before modeling, after modeling, and on the 1st, 4th, and 7th days of treatment. Foot volume was measured to assess toe swelling before modeling, after modeling, and on the 1st and 7th days of treatment. Results:Compared with the control group, the model group exhibited a reduced pain threshold (P < 0.0001) and increased paw volume (P < 0.0001). Compared with the model group, the subgroups receiving moxibustion intervention initiated on the 4th, 7th, and 10th days post-modeling exhibited an increased pain threshold (P < 0.05, P < 0.0001). However, the paw volume of the subgroups receiving moxibustion intervention initiated on the 4th day post-modeling increased (P < 0.0001), while those of the subgroups receiving moxibustion intervention initiated on the 7th and 10th days post-modeling decreased (P < 0.0001). Among the intervention subgroups receiving moxibustion initiated on days 4, 7, and 10, the day 7 intervention-initiating subgroup showed significant increase in pain threshold (P < 0.05, P < 0.0001), and the day 7 and day 10 intervention-initiating subgroups showed significantly reduced paw volume (P < 0.0001). Conclusion:Considering both the analgesic and anti-inflammatory effects of moxibustion, day 7 post-modeling may be the optimal time for moxibustion to achieve effective anti-inflammatory and analgesic outcomes.

Background:Acupuncture and moxibustion, as traditional therapies in Chinese medicine, are widely recognized for their therapeutic effects, particularly in pain relief. Nevertheless, the exact mechanisms underlying their analgesic effects remain to be fully elucidated. Advancements in neuroimaging techniques have opened a novel pathway for investigating alterations in brain function resulting from acupuncture and moxibustion analgesia. Purpose:The purpose of this study was to investigate the brain regions activated during acupuncture and moxibustion treatment for pathological pain using neuroimaging, to better understand the underlying analgesic mechanisms. Patients and Methods:An electronic search of PubMed was conducted using the keywords "acupuncture", "moxibustion", "analgesia", and "neuroimaging". A total of 37 articles, focusing on 14 diseases, were identified and analyzed. Results:Acupuncture primarily activated regions in the frontal, parietal, and temporal lobes, with key areas including the anterior cingulate cortex (ACC), insula, prefrontal cortex (PFC), and primary somatosensory cortex (S1). Different stimulation modes and disease types produced distinct patterns of brain region activation. Conclusion:Acupuncture and moxibustion modulate key brain regions involved in pain perception, emotional regulation, and cognitive functions. Acupuncture predominantly affects the sensory cortex, enhancing pain perception, while moxibustion has a more pronounced effect on the limbic system and thalamus, influencing emotional and cognitive aspects of pain. The findings indicate that acupuncture and moxibustion serve as effective non-pharmacological therapies for pain management, offering valuable insights into their underlying analgesic mechanisms. Future research should focus on further elucidating these mechanisms and optimizing clinical applications.

Background:Acupuncture is widely recognized as the primary form of traditional medical treatment on a global scale, leading to a heightened emphasis on the training and development of proficient acupuncture professionals. The development of proficient practitioners in the field of acupuncture is hindered by the substantial challenges associated with augmenting system integration capabilities for clinical application and active participation in clinical operations. Objective:It is imperative to adhere to a combination of broad and specialized knowledge in order to establish a robust educational base, facilitate effective knowledge transfer, maintain a harmonious emphasis on theoretical understanding, refine practical skills, and improve clinical proficiency. Methods:Embracing collaborative educational strategies, fostering cross-disciplinary integration, and promoting innovative approaches are essential components for enhancing the educational experience in acupuncture. The incorporation of internet, Big Data, artificial intelligence, virtual reality, and other technologies into acupuncture and moxibustion education holds significant importance in advancing the innovation and development of acupuncture education. Conclusion:This article presents practical experiences in integrating digital intelligence with acupuncture talent training at Chengdu University of Traditional Chinese Medicine. The content includes the objectives of acupuncture talent development, a strategic plan for reforming acupuncture talent in practical and classroom teaching, and serves as a valuable reference for acupuncture education.

ABSTRACTAimGiven that electroacupuncture (EA) pretreatment inhibits lactate production and lactate‐derived lysine lactation (Kla) aggravates ischemic brain injury, we aimed to investigate whether the formation of Kla protein is involved in EA pretreatment to alleviate ischemic brain injury.MethodsEA was performed on the Baihui acupoint (GV20) of male C57BL/6J mice before receiving the permanent middle cerebral artery occlusion (pMCAO) surgery. Western blot and immunofluorescent staining were used to observe neuronal survival, astrocyte activation, and protein Kla levels, and the lactate levels in ischemic brains were assayed with a commercial kit. TTC staining and neurological function scores are performed to evaluate the brain damage in mice.ResultsWe found that the increased lactate content and protein Kla levels were significantly decreased in ischemic brain tissue of mice after receiving EA pretreatment, and accompanied by the reduction of astrocyte activation and neuronal injury and death. Meantime, we found that EA pretreatment was effective in reversing the worsening of ischemic brain injury caused by lactate supplementation. However, EA pretreatment did not further reduce the lactate content and protein Kla levels and ameliorate brain injury in ischemic stroke mice after inhibition of glycolysis.ConclusionOur study reveals that EA pretreatment reduced ischemic brain damage by inhibiting lactate production and its derived protein Kla formation in mice with ischemic stroke.