Depression, a prevalent mental disorder with significant socioeconomic burdens, underscores the urgent need for safe and effective non-pharmacological interventions. Recent advances in microbiome research have revealed the pivotal role of gut microbiota dysbiosis in the pathogenesis of depression. Concurrently, exercise, as a cost-effective and accessible intervention, has demonstrated remarkable efficacy in alleviating depressive symptoms. This comprehensive review synthesizes current evidence on the interplay among exercise, gut microbiota modulation, and depression, elucidating the mechanistic pathways through which exercise ameliorates depressive symptoms via the microbiota-gut-brain (MGB) axis. Depression is characterized by gut microbiota alterations, including reduced alpha and beta diversity, depletion of beneficial taxa (e.g., Bifidobacterium, Lactobacillus, and Coprococcus), and overgrowth of pro-inflammatory and pathogenic bacteria (e.g., Morganella, Klebsiella, and Enterobacteriaceae). Metagenomic analyses reveal disrupted metabolic functions in depressive patients, such as diminished synthesis of short-chain fatty acids (SCFAs), impaired tryptophan metabolism, and dysregulated bile acid conversion. For instance, Bifidobacterium longum deficiency correlates with reduced synthesis of neuroactive metabolites like homovanillic acid, while decreased Coprococcus abundance limits butyrate production, exacerbating neuroinflammation. Furthermore, elevated levels of indole derivatives from Clostridium species inhibit serotonin (5-HT) synthesis, contributing to depressive phenotypes. These dysbiotic profiles disrupt the MGB axis, triggering systemic inflammation, neurotransmitter imbalances, and hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. Exercise exerts profound effects on gut microbiota composition, diversity, and metabolic activity. Longitudinal studies demonstrate that sustained aerobic exercise increases alpha diversity, enriches SCFA-producing genera (e.g., Faecalibacterium prausnitzii, Roseburia, and Akkermansia), and suppresses pathobionts (e.g., Desulfovibrio and Streptococcus). For example, a meta-analysis of 25 trials involving 1 044 participants confirmed that exercise enhances microbial richness and restores the Firmicutes/Bacteroidetes ratio, a biomarker of metabolic health. Notably, endurance training promotes Veillonella proliferation, which converts lactate into propionate, enhancing energy metabolism and delaying fatigue. Exercise also strengthens intestinal barrier integrity by upregulating tight junction proteins (e.g., ZO-1, occludin), thereby reducing lipopolysaccharide (LPS) translocation and systemic inflammation. However, excessive exercise may paradoxically diminish microbial diversity and exacerbate intestinal permeability, highlighting the importance of moderate intensity and duration. Exercise ameliorates depressive symptoms through multifaceted interactions with the gut microbiota, primarily via 4 interconnected pathways. First, exercise mitigates neuroinflammation by elevating anti-inflammatory SCFAs such as butyrate, which suppresses NF-κB signaling to attenuate microglial activation and oxidative stress in the hippocampus. Animal studies demonstrate that voluntary wheel running reduces hippocampal TNF‑α and IL-17 levels in stress-induced depression models, while fecal microbiota transplantation (FMT) from exercised mice reverses depressive behaviors by modulating the TLR4/NF‑κB pathway. Second, exercise regulates neurotransmitter dynamics by enriching GABA-producing Lactobacillus and Bifidobacterium, thereby counteracting neuronal hyperexcitability. Aerobic exercise also enhances the abundance of Lactobacillus plantarum and Streptococcus thermophilus, which facilitate 5-HT and dopamine synthesis. Clinical trials reveal that 12 weeks of moderate exercise increases fecal Coprococcus and Blautia abundance, correlating with improved 5-HT bioavailability and reduced depression scores. Third, exercise normalizes HPA axis hyperactivity by reducing cortisol levels and restoring glucocorticoid receptor sensitivity. In rodent models, chronic stress-induced corticosterone elevation is reversed by probiotic supplementation (e.g., Lactobacillus), which enhances endocannabinoid signaling and hippocampal neurogenesis. Furthermore, exercise upregulates brain-derived neurotrophic factor (BDNF) via microbial metabolites like butyrate, promoting histone acetylation and synaptic plasticity. FMT experiments confirm that exercise-induced microbiota elevates prefrontal BDNF expression, reversing stress-induced neuronal atrophy. Fourth, exercise reshapes microbial metabolic crosstalk, diverting tryptophan metabolism toward 5-HT synthesis instead of neurotoxic kynurenine derivatives. Butyrate inhibits indoleamine 2,3-dioxygenase (IDO), a key enzyme in the kynurenine pathway linked to depression. Concurrently, exercise-induced Akkermansia enrichment enhances mucin production, fortifies the gut barrier, and reduces LPS-driven neuroinflammation. Collectively, these mechanisms underscore exercise as a potent modulator of the microbiota-gut-brain axis, offering a holistic approach to alleviating depression through microbial and neurophysiological synergy. Current evidence supports exercise as a potent adjunct therapy for depression, with personalized regimens (e.g., aerobic, resistance, or yoga) tailored to individual microbiota profiles. However, challenges remain in optimizing exercise prescriptions (intensity, duration, and type) and integrating them with probiotics, prebiotics, or FMT for synergistic effects. Future research should prioritize large-scale randomized controlled trials to validate causality, multi-omics approaches to decipher MGB axis dynamics, and mechanistic studies exploring microbial metabolites as therapeutic targets. The authors advocate for a paradigm shift toward microbiota-centric interventions, emphasizing the bidirectional relationship between physical activity and gut ecosystem resilience in mental health management. In conclusion, this review underscores exercise as a multifaceted modulator of the gut-brain axis, offering novel insights into non-pharmacological strategies for depression. By bridging microbial ecology, neuroimmunology, and exercise physiology, this work lays a foundation for precision medicine approaches targeting the gut microbiota to alleviate depressive disorders.

ObjectiveRepetitive transcranial magnetic stimulation (rTMS), a non-invasive brain stimulation technique, offers a non-pharmacological therapeutic option for the management of Alzheimer’s disease (AD). Studies have demonstrated that ferroptosis plays a pivotal role in the pathological onset and progression of AD, and the inhibition of neuronal ferroptosis can significantly ameliorate cognitive impairments associated with AD. The imbalance of calcium ion (Ca²⁺) homeostasis is intimately associated with the pathology of AD and serves as a catalyst for the induction of ferroptosis through various pathways. This study is designed to investigate whether rTMS can ameliorate AD by inhibiting neuronal ferroptosis or maintaining calcium homeostasis, ultimately establishing a theoretical and experimental framework for the utilization of rTMS in AD treatment. MethodsAPP/PS1 AD mice were subjected to both 0.5 Hz low-frequency and 20 Hz high-frequency rTMS treatments, and the efficacy of these treatments was evaluated using novel object recognition and Morris water maze tests. ELISA was employed to quantify the levels of glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), Fe²⁺ within the hippocampi of mice from each group. HT-22 cells were induced to undergo ferroptosis via Erastin treatment, and subsequent to high- and low-frequency magnetic stimulation, cell viability was assessed using CCK-8 assay, while intracellular calcium ion concentration fluctuations were monitored using Fluo-4 AM. ResultsThe findings revealed that, when compared to normal mice, AD mice displayed a notable decline in cognitive function, accompanied by a substantial increase in ferroptosis levels and intracellular calcium ion concentrations. Both high-frequency and low-frequency applications of rTMS were found to significantly ameliorate cognitive impairments in AD mice, while also effectively mitigating the abnormal augmentation of neuronal ferroptosis and intracellular calcium ion levels. ConclusionThe present study underscores that both high-frequency and low-frequency rTMS exhibit efficacy in alleviating cognitive dysfunction in AD mice, potentially through the modulation of ferroptosis and intracellular calcium ion homeostasis.

Aim To explore the effects of Lycium berry seed oil on Nrf2/ARE pathway and oxidative damage in testis of subacute aging rats. Methods Fifty out of 60 male SD rats, aged 8 weeks, were subcutaneously injected with 125 mg • kg"D-galactosidase in the neck for 8 weeks to establish a subacute senescent rat model. The presence of senescent cells was observed using P-galactosidase ((3-gal), while testicular morphology was examined using HE staining. Serum levels of testosterone (testosterone, T), follicle-stimulating hormone ( follicle stimulating hormone, FSH ) , luteinizing hormone ( luteinizing hormone, LH ) , superoxide dis-mutase ( superoxide dismutase, SOD ) , glutathione ( glutathione, GSH) and malondialdehyde ( malondial-dehyde, MDA) were measured through ELISA, and the expressions of factors related to aging, oxidative damage, and the Nrf2/ARE pathway were assessed via immunohistochemical analysis and Western blotting. Results After successfully identifying the model, the morphology of the testis was improved and the intervention of Lycium seed oil led to a down-regulation in the expression of [3-gal and -yH2AX. The serum levels of SOD, GSH, T, and FSH increased while MDA and LH decreased (P 0. 05) . Additionally, there was an up-regulated expression of Nrf2, GCLC, NQOl, and SOD2 proteins in testicular tissue ( P 0. 05 ) and nuclear expression of Nrf2 in sertoli cells. Conclusion Lycium barbarum seed oil may reduce oxidative damage in testes of subacute senescent rats by activating the Nrf2/ARE signaling pathway.

A liquid chromatography-tandem mass spectrometry(LC-MS/MS)method was developed for determination of three kinds of β-agonists(Clenbuterol(CL),Ractopamine(RAC)and Salbutamol(SAL))residues in animal liver samples.The liver sample homogenates were extracted with organic solvent,followed by clean-up using the automatic magnetic solid-phase extraction(MSPE),and then analyzed using LC-MS/MS.The results showed that the magnetic mixed-mode cation exchange adsorbent(M-MCX)exhibited 34%higher adsorption capacity than the conventional mixed-mode cation exchange(MCX)column.Furthermore,the clean-up was conducted by using an automatic MSPE device,and 8 samples could be simultaneously treated within 30 min.The limits of detection(LOD)were 0.01-0.1 μg/kg,the average recoveries ranged from 88.2%to 110.5%,and the relative standard deviations(RSDs)were in range of 2.9%-10.3%at three spiked levels for the three kinds of β-agonists.Compared with the traditional SPE technique,the present method had many advantages such as simple operation,rapidity and high efficiency,which was suitable for high-throughput and automatic detection of residues in routine analysis.

italic>Salmonella has emerged as a promising tumor-targeting strategy in recent years due to its good tumor targeting ability and certain safety. In order to further optimize its therapeutic effect, scientists have tried to modify Salmonella, including its attenuation and drug loading. This paper summarizes the mechanism and research progress of Salmonella-mediated targeted tumor therapy, and introduces the strategies and related progress of its modification and optimization. At the same time, the advantages, current challenges and future development directions of Salmonella-mediated tumor therapy are summarized.

Objective To investigate the effects of tiotropium bromide combined with salmeterol fluticasone on postoperative lung function,blood gas index,and inflammatory response in patients with lung cancer complicated with stable chronic obstructive pulmonary disease(COPD).Methods Patients with lung cancer complicated with stable COPD after surgery were selected as research subjects and divided into control group and treatment group according to different treatment methods.The control group received 18 μg of tiotropium bromide powder for inhalation therapy,bid,for 3 days before surgery,while the treatment group received additional salmeterol inhalation powder treatment on basis of the control group's treatment,1 inhalation each time,bid,for 3 months.Lung function[forced vital capacity(FVC),forced expiratory volume in one second(FEV1),peak expiratory flow(PEF),FEV1/FVC],modified British Medical Research Council(mMRC)dyspnea scale,chronic obstructive pulmonary disease assessment test(CAT)score,quality of life questionnaire-C30(QLQ-C30)score,blood gas index[arterial oxygen pressure(PaO2),arterial blood oxygen saturation(SaO2),arterial carbon dioxide pressure(PaCO2)],inflammatory response indicators[interleukin-6(IL-6),interleukin-8(IL-8),tumor necrosis factor-α(TNF-α)],and occurrence of adverse drug reactions in the two groups with compared before and after treatment.Results Forty-seven and forty-five cases were included in the treatment and control groups,respectively.After treatment,the total effective rates of the treatment and control groups were 91.49％(43 cases/47 cases)and 75.56％(34 cases/45 cases)respectively,and the differences were statistically significant(P＜0.05).After treatment,the FEV1/FVC of the treatment and control groups were(0.62±0.10)％and(0.48±0.05)％;PEF were(1.94±0.20)and(1.02±0.11)L·s-1;mMRC scores were 2.01±0.25 and 2.26±0.23;CAT scores were 16.03±1.74 and 20.03±2.17;QLQ-C30 physical functioning scores were 79.31±8.92 and 75.04±7.86;PaO2 were(70.34±6.98)and(62.02±6.31)mmHg;IL-6 expression levels were(16.43±1.65)and(21.55±2.27)pg·mL-1.The above indexes in the treatment group compared with the control group were all statistically significant(all P＜0.05).The main adverse drug reactions in the treatment and control groups were skin allergies and nausea/vomiting,and the total incidence of adverse drug reactions in the treatment and control groups were 34.04％and 23.40％,with no statistically significant difference(P＞0.05).Conclusion Tiotropium bromide combined with salmeterol fluticasone is effective for patients with lung cancer complicated with stable COPD after surgery,which significantly improves their lung function,prognosis,and arterial blood gas levels.

Objective Recombinase-aided polymerase chain reaction(RAP)is a sensitive,single-tube,two-stage nucleic acid amplification method.This study aimed to develop an assay that can be used for the early diagnosis of three types of bacteremia caused by Staphylococcus aureus(SA),Pseudomonas aeruginosa(PA),and Acinetobacter baumannii(AB)in the bloodstream based on recombinant human mannan-binding lectin protein(M1 protein)-conjugated magnetic bead(M1 bead)enrichment of pathogens combined with RAP. Methods Recombinant plasmids were used to evaluate the assay sensitivity.Common blood influenza bacteria were used for the specific detection.Simulated and clinical plasma samples were enriched with M1 beads and then subjected to multiple recombinase-aided PCR(M-RAP)and quantitative PCR(qPCR)assays.Kappa analysis was used to evaluate the consistency between the two assays. Results The M-RAP method had sensitivity rates of 1,10,and 1 copies/μL for the detection of SA,PA,and AB plasmids,respectively,without cross-reaction to other bacterial species.The M-RAP assay obtained results for<10 CFU/mL pathogens in the blood within 4 h,with higher sensitivity than qPCR.M-RAP and qPCR for SA,PA,and AB yielded Kappa values of 0.839,0.815,and 0.856,respectively(P<0.05). Conclusion An M-RAP assay for SA,PA,and AB in blood samples utilizing M1 bead enrichment has been developed and can be potentially used for the early detection of bacteremia.

Objective To provide a longitudinal evaluation tool based on the frequency of aggressive be-havior for the aggression assessment of schizophrenia patients.Methods The Life History of Aggression was translated and revised to form the Life History of Aggression-Chinese Version(LHA-CV)based on 369 patients diagnosed with schizophrenia in the Chengdu community and compulsory medical insti-tution.The reliability of LHA-CV was analyzed by means of split-half reliability,test-retest reliability and inter-evaluator consistency.The validity was analyzed by item analysis,construct validity and crite-rion validity.Results Item analysis found that LHA-CV had good homogeneity and discriminant validity.Exploratory factor analysis found that the Kaiser-Meyer-Olkin(KMO)test value was 0.80,and the Bartlett's sphericity test χ2=1203.46(P<0.05),and it revealed four factors including non-physical ag-gression,physical aggression,self-directed aggression and antisocial behavior/consequences.The factor loadings for all 11 items were greater than 0.40.Confirmatory factor analysis was performed on the factor model,Chi-square degree of freedom(χ2/df)was 3.61,root mean square error of approxima-tion(RMSEA)was 0.07,goodness-of-fit index(GFI)was 0.92,comparative fit index(CFI)was 0.90,incremental fit index(IFI)was 0.90,and the discriminant validity of each factor was good.The criterion validity test showed the total score of LHA-CV was positively correlated with the aggressive behavior level of MacArthur Community Violence Instrument,the total score of Buss-Perry Aggression Scale,and the score of Antisocial Personality Disorder Subscale of Personality Diagnostic Question-naire-4th Edition Plus(PDQ-4+_ASPD,P<0.05).The Cronbach's α coefficient of non-physical aggres-sion,physical aggression,self-directed aggression,antisocial behavior/consequences and LHA-CV total score were 0.82,0.73,0.74,0.56 and 0.79,respectively.The test-retest reliability,Spearman-Brown split-half reliability and intra-class correlation coefficient of LHA-CV total score were 0.82(P<0.05),0.66 and 0.99,respectively.Conclusion LHA-CV has good reliability and validity,and can be used as an evaluation tool for longitudinally assessing aggressive behavior in schizophrenia patients.

Yellowish sweating disease is one of the fluid-retention diseases recorded in Jin Gui Yao Lve(Synopsis of the Golden Cabinet).The symptoms of yellowish sweating disease are complex,involving multiple visceral lesions,which are caused by interior heat and exterior deficiency,together with the concurrent invasion of pathogens of wind and water.Huangqi Shaoyao Guizhi Kujiu Decoction(mainly composed of Astragali Radix,Paeoniae Radix Alba,Cinnamomi Ramulus and vinegar)and Guizhi Plus Huangqi Decoction(mainly composed of Cinnamomi Ramulus and Astragali Radix)are the classical formula for the treatment of yellowish sweating disease.Both of the formulas have the actions of warming defensive qi and dredging yang,removing fluid retention and resolving dampness.Usually suffering heat in the spleen and stomach,together with carelessness in daily living and wind-water pathogens attacking the exterior,contributes to the key pathogenesis of diabetes mellitus.The clinical manifestations,etiology,occurrence and progression,and prognosis of yellowish sweating disease are similar to those of diabetic complications.Therefore,the treatment of diabetes complications such as diabetic kidney disease,diabetic cardiomyopathy,diabetic peripheral neuropathy,diabetes mellitus complicated with liver dysfunction,diabetic foot,and diabetic retinopathy can follow the therapeutic principles of yellowish sweating disease,and can be achieved by the therapies of clearing heat and purging fire,dispelling cold and removing dampness,and nourishing nutritive yin and harmonizing defensive qi with the appropriate formulas.The exploration of the treatment of diabetes mellitus and its complications from the pathogenesis and symptom characteristics of yellowish sweating disease will expand the thoughts for treating diabetic complications with traditional Chinese medicine.

Objective To explore the changes in gut microbiota and levels of short-chain fatty acids(SCFA)in infants with cow's milk protein allergy(CMPA),and to clarify their role in CMPA.Methods A total of 25 infants diagnosed with CMPA at Children's Hospital Affiliated to Zhengzhou University from August 2019 to August 2020 were enrolled as the CMPA group,and 25 healthy infants were selected as the control group.Fecal samples(200 mg)were collected from both groups and subjected to 16S rDNA high-throughput sequencing technology and liquid chromatography-mass spectrometry to analyze the changes in gut microbial composition and metabolites.Microbial diversity was analyzed in conjunction with metabolites.Results Compared to the control group,the CMPA group showed altered gut microbial structure and significantly increased α-diversity(P＜0.001).The abundance of Firmicutes,Clostridiales and Bacteroidetes was significantly decreased,while the abundance of Sphingomonadaceae,Clostridiaceae_l and Mycoplasmataceae was significantly increased in the CMPA group compared to the control group(P＜0.001).Metabolomic analysis revealed reduced levels of acetic acid,butyric acid,and isovaleric acid in the CMPA group compared to the control group,and the levels of the metabolites were positively correlated with the abundance of SCFA-producing bacteria such as Faecalibacterium and Roseburia(P＜0.05).Conclusions CMPA infants have alterations in gut microbial structure,increased microbial diversity,and decreased levels of SCFA,which may contribute to increased intestinal inflammation.[Chinese Journal of Contemporary Pediatrics,2024,26(3):236-243]