ObjectiveTo investigate the role and underlying mechanism of the Wnt/β-catenin signaling pathway in the process of Xiaojinwan （XJW）-containing serum interfering with endothelial-mesenchymal transition （EMT） in human breast cancer MDA-MB-231 cells. MethodsXJW-containing serum was prepared by intragastric administration of XJW （4 g·kg^-1） to SD rats. MDA-MB-231 cells were cultured in vitro. β-Catenin overexpression and knockdown plasmids were constructed and transfected into MDA-MB-231 cells. The optimal XJW-containing serum （4 g·kg^-1） according to previous studies was used for β-catenin intervention and overexpression experiments. The groups for intervention/overexpression experiments included intervention/overexpression blank group， β-catenin intervention/overexpression group， intervention/overexpression blank + XJW group， and β-catenin intervention/overexpression + XJW group. Cell morphology was observed under a microscope. Flow cytometry was used to detect and record apoptosis rates. Western blot was performed to measure apoptosis-related proteins ［B-cell lymphoma 2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and active-Caspase-3］ and EMT-related proteins （E-cadherin， N-cadherin， and vimentin）. Real-time polymerase chain reaction （Real-time PCR） was used to detect β-catenin mRNA expression levels in different groups. ResultsIntervention experiment results showed that compared with the intervention blank group， the β-catenin intervention group and the intervention blank + XJW group showed increased apoptosis rates （P<0.05， P<0.01）， elevated protein levels of Bax， active Caspase-3， and E-cadherin （P<0.05， P<0.01）， and decreased protein levels of Bcl-2 and Vimentin （P<0.05， P<0.01）. β-catenin mRNA expression was reduced in the β-catenin intervention group （P<0.05， 0.63 ± 0.15） and the intervention blank + XJW group （P<0.05， 0.79 ± 0.33）. Compared with the β-catenin intervention group， the β-catenin intervention + XJW group exhibited an increased apoptosis rate （P<0.01）， elevated Bax and active Caspase-3 protein levels （P<0.05， P<0.01）， and decreased Bcl-2， N-cadherin， and Vimentin protein levels （P<0.05）. β-catenin mRNA expression was further reduced in the β-catenin intervention + XJW group （P<0.01， 0.22 ± 0.08）. Compared with the intervention blank + XJW group， the β-catenin intervention + XJW group showed an increased apoptosis rate （P<0.01）， elevated Bax， active Caspase-3， and E-cadherin protein levels （P<0.05， P<0.01）， and decreased Bcl-2， N-cadherin， and vimentin protein levels （P<0.05， P<0.01）. β-catenin mRNA expression was also reduced （P<0.05）. Overexpression experiment results showed that compared with the overexpression blank group， the β-catenin overexpression group exhibited a reduced apoptosis rate （P<0.01）， while the overexpression blank + XJW group showed an increased apoptosis rate （P<0.05）. In the β-catenin overexpression and β-catenin overexpression + XJW groups， Bax and E-cadherin protein levels decreased （P<0.05， P<0.01）， while Bcl-2， N-cadherin， and vimentin levels increased （P<0.05）. In the overexpression blank + XJW group， Bax and E-cadherin levels increased （P<0.05， P<0.01）， while Bcl-2， N-cadherin， and vimentin levels decreased （P<0.05， P<0.01）. β-catenin mRNA expression increased in the β-catenin overexpression group （P<0.01， 7.26 ± 1.03） but decreased in the overexpression blank + XJW group （P<0.05， 0.73 ± 0.14）. Compared with the β-catenin overexpression group， the β-catenin overexpression + XJW group showed an increased apoptosis rate （P<0.01）， elevated Bax and E-cadherin levels （P<0.05）， and decreased N-cadherin and vimentin levels （P<0.05）. β-catenin mRNA expression was reduced （P<0.05， 4.65 ± 1.02）. Compared with the overexpression blank + XJW group， the β-catenin overexpression + XJW group exhibited a reduced apoptosis rate （P<0.01）， decreased Bax and E-cadherin levels （P<0.01）， and increased Bcl-2， N-cadherin， and Vimentin levels （P<0.05）. β-catenin mRNA expression increased （P<0.01）. ConclusionXJW-containing serum inhibits breast cancer cell proliferation by suppressing EMT， which is associated with the regulation of the Wnt/β-catenin pathway.

Acute lung injury （ALI） is a critical respiratory emergency caused by various non-cardiogenic factors， including severe pulmonary and extrapulmonary infections， lung contusion， and sepsis. Its pathological features are centered on alveolar-capillary barrier dysfunction， uncontrolled inflammatory responses， and impaired alveolar fluid clearance， manifesting as refractory hypoxemia and respiratory distress， with a poor clinical prognosis. Modern studies have revealed that mitochondrial dysfunction and glucose metabolic reprogramming in macrophages， characterized by hyperactivated glycolysis， drive pro-inflammatory polarization and represent a key mechanism leading to excessive inflammatory responses and disease progression in ALI. Therefore， targeting macrophage glycolysis may be a potential therapeutic strategy for ALI. The Plain Questions： Special Discussion on Channels and Vessels in Huangdi's Internal Classic states that "The spleen disseminates essence upward to the lungs". When the spleen fails in transport and transformation， the distribution of refined nutrients becomes disordered， resulting in the endogenous generation of turbid pathogens that obstruct the pulmonary collaterals， causing failure of lung dispersion and descent and leading to dyspneic reversal. This forms the dynamic pathological pattern of ''deficiency in the root with excess in the manifestation''， thereby proposing the core pathogenesis of ALI as ''spleen deficiency with transport dysfunction and turbid pathogens obstructing the lungs''. This process is intrinsically associated with the inflammatory cascade triggered by disordered macrophage glucose metabolism. Taking the theory of ''spleen failing to disperse essence'' as the entry point， the present study systematically elucidates the progressive pathological mechanism of "energy metabolism disorder-cytokine storm'' in ALI from the perspectives of the ''spleen deficiency-turbid obstruction'' pathogenesis and macrophage glycolysis-pro-inflammatory polarization. In addition， we summarize Chinese medicine compound formulas and monomeric components that ''restore spleen transport and eliminate turbid pathogens''， and explore their potential mechanisms in the treatment of ALI by regulating macrophage metabolic phenotypes to improve the state of ''spleen failing to disperse essence''. This provides a molecular basis for elucidating the ''spleen-lung'' energy metabolism dialogue， deepens understanding of the multi-target regulatory mechanisms of herbal prescriptions， and promotes the deep integration of classical theory with modern medicine.

Psychological problems are significant factors that contribute to the occurrence of postoperative complications, reduced quality of life, and prolonged hospital stays. Lung cancer patients who require surgery often experience high psychological stress related to both the disease and the treatment, making them more susceptible to depression and anxiety. Therefore, timely intervention to address these psychological issues is crucial for promoting postoperative recovery and improving patients' quality of life. This paper will review the current status, impact, and interventions for depression and anxiety-related psychological problems in lung cancer surgery patients.

Bone marrow suppression is one of the common adverse reactions to radiotherapy and chemotherapy. Anticancer treatments such as radiotherapy and chemotherapy first directly damage the patient′s peripheral blood cells, impairing qi and blood; further, they damage the actively proliferating cell populations in the bone marrow, impairing yin and blood; and then they interfere with hematopoietic stem cells, impairing essence and blood. This process is rapid and intense, consistent with the characteristics of " acute deficiency syndrome" , marked by sudden onset, rapid changes, critical condition, complexity and variability, multiple complications, and poor prognosis. Given this, its diagnosis and treatment should differ from those of general deficiency syndromes. This paper advocates the principles and ideas of diagnosis and treatment such as " preventing first and treating early to prevent changes; supplementing for deficiency and strengthening vital qi to eliminate pathogenic factor; urgent rescue for critical conditions, no time to lose; and comprehensive supplementing throughout the process, with severe cases requiring singular action" . This approach is intended to provide theoretical reference and practical guidance for bone marrow suppression after radiotherapy and chemotherapy.

Precancerous lesions of gastric cancer （PLGC） are a group of pathological changes caused by abnormalities in the structure， morphology， and differentiation of gastric mucosal epithelial cells. Since the early symptoms are hidden and non-specific， PLGC is not easy to be diagnosed and it has often developed into intermediate or advanced gastric cancer once being diagnosed and missed the best time for treatment. Accordingly， the incidence of this disease is increasing year by year， which lifts a heavy burden on the patients. The pathogenesis of PLGC is complex， involving inflammatory microenvironment， bile reflux， glycolysis， autophagy， and apoptosis. Currently， PLGC is mainly treated with anti-inflammatory and endoscopic therapies， which are difficult to curb the development of PLGC. Therefore， seeking a safe and effective therapy is an important topic of modern research. Traditional Chinese medicine （TCM）， characterized by treatment based on syndrome differentiation and a holistic view， exerts effects via multiple pathways， mechanisms， and targets. Recent studies have confirmed that TCM can regulate the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR）， Wnt/β-catenin， Sonic Hedgehog， nuclear factor-κB （NF-κB）， Janus kinase/signal transducer and activator of transcription （JAK/STAT）， hypoxia-inducible factor-1α （HIF-1α）， neurogenic locus notch homolog protein （Notch）， nuclear factor E₂-related factor 2 （Nrf2） and other signaling pathways. By targeting these pathways， TCM can inhibit aerobic glycolysis， reduce oxidative stress， repair the inflammatory microenvironment， regulate cellular autophagy， and promote vascular normalization， thereby delaying or reversing PLGC. However， few researchers have systematically summarized the TCM regulation of PLGC-associated pathways. By reviewing the relevant articles at home and abroad， this paper summarized the roles of the above signaling pathways in the development of PLGC and the research progress in the regulation of signaling pathways by TCM in the treatment of PLGC， with a view to providing a new theoretical basis for the clinical research on PLGC and the drug development for this disease.

Objective To investigate the therapeutic effects and mechanisms of electroacupuncture(EA)at"Baihui"(GV20)and"Shenting"(GV24)acupoints in a rat model of insomnia.Methods An insomnia model was established by intraperitoneal injection of para-chlorophenylalanine(PCPA).Thirty-six rats were randomly divided into four groups(n=9 each):normal control group,EA-treated normal,model,and EA-treated model group.After successful modeling,EA intervention was administered for 7 days.Sleep duration and quality were monitored using an animal sleep-phase analysis system.Hypothalamic levels of serotonin(5-HT),dopamine(DA),tumor necrosis factor α(TNF-α),interleukin 6(IL-6),inducible nitric oxide synthase(iNOS),mannose receptor(CD206),interleukin 10(IL-10),and arginase 1(ARG1)were measured by ELISA.Hypothalamic histopathology was assessed via hematoxylin-eosin(HE)staining.Western Blot analyzed brain-derived neurotrophic factor(BDNF)and its receptor tropomyosin kinase B(TrkB)protein expression.Results Compared with the normal group,rats in the model group exhibited hypothalamic tissue damage,accompanied by reduced 5-HT levels,elevated DA concentrations,and significantly impaired sleep duration and sleep quality scores(P＜0.05).Concurrently,the model group showed increased levels of M1 microglial markers(TNF-α,IL-6,iNOS)but decreased levels of M2 markers(CD206,IL-10,ARG1),alongside diminished protein expression of both BDNF and TrkB in the hypothalamus,the difference being statistically significant(P＜0.05).In contrast,the EA-treated model group demonstrated attenuated hypothalamic lesions relative to the untreated model group.These rats exhibited elevated 5-HT levels,reduced DA concentrations,and significantly improved sleep duration and quality(P＜0.05).Furthermore,EA treatment decreased expression of M1 markers(TNF-α,IL-6,iNOS)while increasing M2 markers(CD206,IL-10,ARG1),with concomitant upregulation of BDNF and TrkB protein expression,the difference being statistically significant(P＜0.05).Conclusion EA at"Baihui"and"Shenting"alleviates insomnia symptoms by promoting microglial M1-to-M2 polarization,potentially via BDNF/TrkB pathway activation.

Sepsis is a life-threatening acute organ dysfunction syndrome caused by a dys-regulated host response to infection.As a regenerative medicine therapy with broad clinical prospects,stem cells have attracted significant at-tention due to their multifaceted biological capabilities,including anti-inflammatory,antioxidant,and anti-apoptotic effects,as well as immunomodulatory properties and tissue/organ repair potential.Mesenchymal stem cells(MSCs)function through mechanisms such as modulating macrophage polarization and suppressing excessive inflammation responses,thereby promoting tissue regeneration.Pre-clinical studies demonstrate that MSCs significantly reduce sepsis mortality and decrease sepsis-associated complications including acute kidney injury(AKI),acute respiratory distress syndrome(ARDS)and sepsis associated myopathy.Furthermore,perinatal-derived stem cells and genetically modified stem cells have shown therapeutic promise in sepsis management.Current challenges in stem cell-based sepsis therapy cover optimizing delivery strategies,standardizing cell preparation protocols and de-veloping biomarker-guided personalized therapeutic regimens.

Objective To investigate the impact of various health education intervention strategies on the proper use of personal respiratory protective equipment (RPE) among workers exposed to dust. Methods Dust-exposed workers were recruited from 60 selected enterprises in Guangdong Province using cluster random sampling method. They were randomly allocated to the control, low-intensity intervention, and high-intensity intervention groups, with 358, 346, and 371 workers in each group, respectively. Workers in the control group received no designed intervention. Workers in the low-intensity intervention group received traditional plus mobile health education on the proper use of RPE. Workers in the high-intensity intervention group received all components of the low-intensity intervention, supplemented with peer education. The intervention lasted for six months. RPE usage was compared among the three groups of workers before and after the intervention. Results Workers in the control, low-intensity intervention, and high-intensity intervention groups showed higher rates of both RPE wearing and correct RPE wearing after the intervention than before it within their respective groups (RPE wearing rate: 94.1% vs 99.2%, 95.7% vs 100.0%, 94.6% vs 100.0%, all P<0.01; correct RPE wearing rate: 66.8% vs 91.1%, 67.3% vs 95.7%, 66.6% vs 96.5%, all P<0.01). Post-intervention correct RPE wearing rates were highest in the high-intensity intervention group, followed by the low-intensity intervention group, and the control group, with the percentage of 96.50%, 95.66% and 91.06%, respectively (P<0.01). Binary logistic regression analysis result showed that different intervention strategies affected the correct use of personal RPE among dust-exposed workers after adjusting for gender, age, and other confounding factors (P<0.05). Compared with the control group, the rates of correct RPE use increased in the low-intensity intervention group and the high-intensity intervention group (odd ratio was 2.14 and 3.01; 95% confidence interval was 1.12 - 4.10 and 1.53 - 5.91, respectively). Conclusion The implementation of traditional plus mobile health education interventions on the proper use of RPE can promote correct RPE utilization among dust-exposed workers, and integrating peer education further enhances the intervention effectiveness.

Accurate characterization of the chemical composition of complex traditional Chinese medicine (TCM) is an essential foundation for the modern scientific interpretation of TCM principles. Mass spectrometry is the most dominant technique in current research on the material basis of TCM, offering the highest sensitivity and the richest information provision. Establishing mass spectrometry databases represents the most effective approach to facilitating the structural analysis of TCM chemical components. This paper systematically searches and reviews literature published from January 2005 to January 2025 through online databases such as China National Knowledge Infrastructure, PubMed, and Web of Science, using “mass spectrometry database” and “traditional Chinese medicine” as keywords. It reviews the current status of seven TCM chemical component mass spectrometry databases and seven natural product mass spectrometry databases. The key advancements of these mass spectrometry databases for natural products are summarized, detailing their characteristics, search methodologies, included information, and data sources. Additionally, challenges related to data quality, standardization, timely updates, database interaction, retrieval functionality, and data sharing and security are discussed in depth. Furthermore, the paper explores prospective development directions for TCM mass spectrometry databases, emphasizing the importance of open data sharing, technological innovation, and data security. Through this analysis, the paper aims to offer theoretical guidance and practical recommendations for the precise identification of TCM components, as well as for the construction and application of these databases.

Energy metabolism reprogramming is one of the pathological mechanisms involved in the occurrence and development of tumors.This article focused on the theory of spleen deficiency in TCM and energy metabolism reprogramming to elaborate the pathological mechanism of tumors.TCM believes that spleen deficiency is an important organ pathogenesis that causes cancer due to deficiency,and spleen deficiency runs through the occurrence and development of tumors.The spleen is the source of qi and blood transformation and dominates the energy metabolism of the whole body.Mitochondria are the regulatory center of energy metabolism in the body,and abnormal mitochondrial energy metabolism is the manifestation of spleen deficiency at the cellular micro level,which is mainly manifested as the limitation of mitochondrial oxidative phosphorylation and the conversion to aerobic glycolysis to provide energy for the rapid growth of tumors.Therefore,based on the theory of spleen deficiency,the treatment based on spleen strengthening is used to prevent and treat tumors by improving energy metabolism,which not only enriches the modern medical connotation of spleen deficiency in TCM,but also provides a new perspective for TCM to treat malignant tumors from the perspective of spleen strengthening.