Objective: To analyze the relationship of gross motor skills and perceptual motor abilities with physical activity levels in preschool children in a Beijing kindergarten, so as to provide a reference for promoting the development of motor competence. Methods: From September 2018 to March 2021, preschoolers aged 4-5 years were selected using convenience sampling method from an urban kindergarten in Beijing. The Test of Gross Motor Development-Third Version(TGMD-3) was used to assess basic preschoolers s gross motor skills ( n =152). The Pictorial Scale of Perceived Movement Skill Competence(PMSC) was used to evaluate perceptual motor skills ( n =151). Accelerometers (Actigraph GT3X) were used to record physical activity levels ( n =52). Data were analyzed using one way analysis of variance (ANOVA) and Pearson correlation coefficients. Results: The mean scores for gross motor skills and perceptual motor abilities were (38.76±13.48) and (35.49±6.50), respectively. The moderate to vigorous physical activity(MVPA) level was(52.60±27.44) minutes per day. No statistically significant correlations were found between gross motor skills, perceptual motor abilities MVPA among boys, girls or the overall group ( r =-0.20 to 0.25, all P >0.05). However, Boys locomotor skills, overall children s locomotor skills, and boys gross motor skills were all positively correlated with MVPA( r =0.34-0.45, all P <0.05). Conclusion There is a correlation between locomotor skills and physical activity levels in 4 to 5-year-old children.

Optical coherence tomography angiography(OCTA)is an innovative non-invasive imaging technology that enables non-invasive, layered, and three-dimensional quantitative visualization of the retinal and choroidal capillary networks by detecting blood flow signals in a contrast-free manner. With its non-invasiveness, high resolution, and quantifiability, OCTA demonstrates significant potential in disease screening, precise staging, treatment decision-making, and prognosis prediction. Its core advantage lies in the accurate quantification of key microcirculation parameters, such as vessel density(VD), non-perfusion area(NPA), foveal avascular zone(FAZ)morphology, and neovascular activity. In diabetic retinopathy(DR), retinal vascular occlusive diseases(RVO/RAO), age-related macular degeneration(ARMD), and glaucoma, OCTA can sensitively detect reduced vessel density in the deep capillary plexus before clinically visible lesions appear, providing a basis for early screening and risk stratification. Additionally, OCTA has shown important value in managing uveitis, pathological myopia, and other ocular conditions. This review systematically elaborates on the technical principles, key quantitative parameters, and core application value of OCTA in the management of various ophthalmic diseases and presents scientific prospects for the application of OCTA in standardized ophthalmic treatment. With further advancements in hardware scanning speed, wide-field imaging capabilities, artificial intelligence algorithms, and multi-modal integration, OCTA is expected to become an essential component of standard ophthalmic diagnosis and treatment. It may also provide a non-invasive window for microcirculation research in neurological and systemic diseases.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

Chronic heart failure （CHF） is a complex clinical syndrome that the cardiac output is not enough to meet the metabolic needs of the body， or depends on the increase of filling pressure to compensate. Its high morbidity and mortality pose a serious threat to human health， necessitating attention and active intervention. At present， western medicine treatment of CHF is mainly based on diuretics， intravenous vasodilators， intravenous positive inotropic drugs， etc.， which， however， have problems such as long medication cycles， serious side effects， and limited applicable population. Recent studies have shown that traditional Chinese medicine can act in a multi-pathway， multi-component， and multi-target manner， showing unique advantages in the prevention and treatment of CHF. Buyang Huanwutang has the effects of tonifying Qi， activating blood， and dredging collaterals. Clinical and mechanism studies have confirmed that this prescription is effective in treating CHF and its syndromes. The clinical studies can be classified into two categories. Studies of the first category use simple modern medical diagnostic criteria as the inclusion criteria for CHF patients， which can improve the scientificity and objectivity. Studies of the second category uses modern medicine combined with traditional Chinese medicine disease diagnostic criteria for the screening of CHF patients， which helps to improve the accuracy of efficacy evaluation. However， there are problems such as the lack of unified research standards and the insufficiency of mechanism research. In addition， the available studies remain to be classified or summarized. This study systematically sorted out the clinical and mechanism studies of Buyang Huanwutang in the treatment of CHF in recent years to review the research status. In clinical treatment， Buyang Huanwutang can be used alone， or modified， or combined with other prescriptions or Western medicine. The mechanism studies predict that Buyang Huanwutang can ameliorate CHF by regulating the calcium balance， protecting the mitochondrial structure and function， and regulating intestinal flora. This review aims to provide a theoretical basis and practical guidance for the clinical application and optimization and subsequent in-depth study of Buyang Huanwutang in the treatment of CHF.

Objective To explore the mediating effect of sleep quality between somatic symptoms and severity of depression in patients with depression. Methods A total of 384 drug-naive patients diagnosed with depression were recruited from the Department of Psychological Medicine of Zhongshan Hospital, Fudan University, during the period from February to August 2024. The severity of depression, somatic symptoms, and sleep quality were assessed using Patient Health Qusetionaire (PHQ)-9, PHQ-15, and Pittsburgh sleep quality index (PSQI), respectively. Based on the PHQ-15 scores, all participants were stratified into two groups: a mild somatic symptoms group（＜10 points, n＝136）and a moderate-to-severe somatic symptoms group（≥10 points, n＝248）. Comparisons of sleep quality between the two groups were conducted, and partial correlation analysis was performed to examine the correlation between sleep quality and somatic symptoms. Additionally, linear regression and mediation analyses were conducted to investigate the mediating effect of sleep quality between somatic symptoms and severity of depression. Results The PSQI scores in moderate-to-severe somatic symptoms group were significantly higher than those in mild somatic symptoms group (P＜0.001). Partial correlation analysis indicated that, after controlling for depression severity, the positive correlation between PSQI and PHQ-15 scores remained significant in both groups (P＜0.01). Regression analysis identified both sleep quality and somatic symptoms as predictors of severity of depression (P＜0.001). Additionally, mediation analysis demonstrated that sleep quality partially mediated the relationship between somatic symptoms and severity of depression, accounting for 26.63% (0.090/0.338) of the total effect. Conclusions In patients with depression, sleep quality is associated with somatic symptoms, and both contribute to an increased risk of the severity of depression. Moreover, sleep quality plays a partial mediating effect between somatic symptoms and severity of depression, highlighting the importance of addressing sleep-related issues in the management of depression.

Objective : To observe the brain tissue injury during hypoxia-ischemia, as well as the pathological changes and the expression of ferroptosis-related factors after the use of Shenfu injection(SFI), and to explore the protective effect of SFI on hypoxic-ischemic brain injury(HIBD) by inhibiting ferroptosis. Methods : An animal model of HIBD in SD rats was constructed and intervened with SFI. Pathologic changes in brain tissue were observed by HE staining methods. Nissen staining was used to observe neuron survival. Glutathione Peroxidase 4(GPX4) and Divalent Metal Transporter 1(DMT1) expression were detected in brain tissue by Western blot, immunohistochemistry and immunofluorescence. Reduced Glutathione(GSH), Lactate Dehydrogenase(LDH), Malondialdehyde(MDA), Superoxide Dismutase(SOD) and tissue iron content were determined with the kits. BV-2 microglial cell line(BV2) cells were culturedin vitroand divided into control group(Ctrl group), oxygen-glucose deprivation group(OGD group), iron ferroptosis-inducing group(Erastin group), iron ferroptosis-inhibiting group(Fer-1 group), Shenfu injection group(SFI group), and Erastin+Shenfu injection group(Erastin+SFI group). 2′,7′-Dichlorodihydrofluorescein diacetate(DCFH-DA) reactive oxygen species(ROS) fluorescent probe was used to detect the ROS release level; Immunofluorescence was used to observe intracellular GPX4, DMT1 expression. Results : Compared with the Sham group, rats in the HIBD group showed significant neuronal cell damage in brain tissue, decreased GPX4 expression(P<0.01), increased DMT1 expression(P<0.01), decreased GSH and SOD levels(P<0.01), and increased LDH, MDA and tissue iron levels(P<0.05,P<0.05,P<0.01). In contrast, after the intervention of SFI, GPX4 expression was elevated(P<0.01), DMT1 expression decreased(P<0.01), GSH and SOD levels were elevated(P<0.01), and LDH, MDA, and tissue iron levels decreased(P<0.05,P<0.05,P<0.01). The cells experiments showed that compared with the Ctrl group, the OGD group had a significantly higher ROS content and a decrease in the expression of GPX4 fluorescence intensity, and an increase in the fluorescence intensity of DMT1(P<0.01), compared with the OGD group, the ROS content was reduced in the SFI group, while the expression of GPX4 was elevated and the expression of DMT1 was reduced(P<0.01). Conclusion Hippocampal and cortical regions are severely damaged after HIBD in neonatal rats, and their brain tissues show decreased expression of GPX4 and increased expression of DMT1. The above suggests that ferroptosis is involved in HIBD brain injury in neonatal rats. In contrast, Shenfu injection has a protective effect on HIBD experimental animal model and BV2 cell injury model by reducing iron aggregation and ROS production.

Objective:To explore the role of curcumin (Cur) in improving IgA nephropathy (IgAN) and its related mechanisms.Methods:Fifty 7-month-old miR-23b knockout (miR-23b -/-) mice weighing (25±5) g were used to establish an IgAN disease model, and were randomly divided into IgAN group, IgAN+Cur (150 mg/kg) group and IgAN+Cur (300 mg/kg) group using simple randomisation. Sixteen healthy 7-month-old weighing (25±3) g C57BL/6J wild-type mice served as the normal control group. IgAN+Cur (150 mg/kg) and IgAN+Cur (300 mg/kg) groups were respectively gavaged continuously with 150 mg/kg Cur and 300 mg/kg Cur for 8 weeks, and the normal control and IgAN groups were gavaged continuously with an equal dose of 0.9% sodium chloride solution for 8 weeks. The samples of urine, serum, intestinal fluid, intestinal tissues, kidney tissues and liver tissues were collected from each group. In vitro experiments, human cloned colon adenocarcinoma (Caco-2) cells were divided into blank control (Ctrl), Ctrl+Cur (10 μmol/L), Ctrl+ Cur (60 μmol/L), tumor necrosis factor-α（TNF-α), TNF-α+Cur (10 μmol/L) and TNF-α+Cur (60 μmol/L) groups. Enzyme-linked immunosorbent assay was used to detect serum alanine transaminase, aspartate transaminase, secretory IgA (sIgA), creatinine, blood urea nitrogen, 24 h urine microalbumin, as well as sIgA, TNF-α, interleukin（IL)-6 and IL-1β in the intestinal fluids. HE staining was used to observe the effect of Cur on liver tissues, the hyperplasia of glomerular mesangial zone in kidney tissues and the morphological and structural changes of intestinal epithelial barrier, and the histopathological damage scores were performed respectively. PAS staining was used to observe the changes of glomerular basement membrane and mesangial matrix. Immunofluorescence was used to observe the deposition of immune complexes in the glomerular mesangial zone. Real-time quantitative PCR was used to detect the mRNA expression levels of B-cell activating factor ( BAFF) and a proliferation inducing ligand ( APRIL). Western blotting was used to detect the protein expression levels of tight junction proteins zonula occluden-1 (ZO-1) and occludin in the mouse intestinal tissues. The potential targets of Cur in IgAN were predicted. Western blotting was used to detect the protein expression levels of tight junction proteins, as well as Toll-like receptor 9 (TLR9), myeloid differentiation primary response protein (MyD88), nuclear factor-κB p65 (NF-κB p65) and p-NF-κB p65. Results:Genetic identification results revealed that all IgAN model mice exhibited the miR-23b -/- genotype, confirming successful model establishment. Seven-month-old mice were subsequently selected for Cur treatment. Histopathological analysis demonstrated no significant differences in hepatic tissue morphology across groups, with comparable liver histopathological injury scores and unaltered liver function parameters, thereby validating the safety of Cur administration. Compared with the normal control group, IgAN mice displayed elevated levels of serum sIgA, serum creatinine, blood urea nitrogen and 24 h urine microalbumin (all P<0.05). Renal pathological results revealed severe mesangial hypercellularity in glomeruli, higher glomerular injury scores, and notable glomerular mesangial deposits of IgA, IgG and complement C3 in IgAN mice (all P<0.05). Additionally, intestinal pathological alterations were observed, including structural changes in intestinal epithelium and Peyer's patches, accompanied by significantly higher intestinal histopathological injury scores in IgAN mice ( P<0.05). Intestinal epithelial expression levels of ZO-1 and occludin were significantly reduced, while sIgA, TNF-α, IL-1β and IL-6 in intestinal fluid were elevated (all P<0.05). Serum FITC fluorescence intensity was markedly increased, and intestinal tissue exhibited upregulated mRNA expression of BAFF and APRIL (all P<0.05). Following Cur treatment, serum sIgA level and renal function indices in mice showed partial recovery (all P<0.05). Renal pathological improvements included alleviated mesangial hypercellularity, reduced glomerular injury scores, and diminished glomerular immune complex deposition (all P<0.05). Intestinal pathologies, including epithelial and Peyer's patch lesions, were mitigated, with decreased intestinal histopathological injury scores ( P<0.05). Additionally, intestinal tight junction protein expression levels were upregulated, intestinal fluid sIgA level was reduced, inflammatory markers were attenuated, serum FITC fluorescence intensity was declined, and intestinal BAFF and APRIL mRNA expression levels were downregulated (all P<0.05). In vitro experiments demonstrated that TNF-α exposure reduced tight junction protein expression in Caco-2 cells, whereas Cur treatment reversed the effect (all P<0.05). Target prediction analysis revealed that Cur effectively bound to TLR9 structural domain in IgAN. Experimental validation confirmed that Cur treatment suppressed the upregulated protein expression levels of TLR9, MyD88, NF-κB p65 and p-NF-κB p65 in intestinal tissues of IgAN mice (all P<0.05). Conclusion:Cur has a significant effect in the treatment of IgAN and can regulate intestinal mucosal immunity by inhibiting the TLR9/MyD88/NF-κB signaling pathway, thereby reducing renal injury and protecting the kidneys.

This report described the diagnosis and management of a case of multiple synostosis syndrome type 3 associated with a variant in the fibroblast growth factor 9 ( FGF9) gene. The neonate presented characteristic features at birth including limited flexion-extension of the right elbow, left talipes equinovarus, frontal bossing, and craniosynostosis. Whole-exome sequencing identified a heterozygous missense variant FGF9 c.566C>G (p.Pro189Arg), subsequently confirmed by Sanger sequencing as maternally inherited. This specific variant has not been previously reported in association with craniosynostosis. The infant underwent staged bilateral craniosynostosis surgeries at 2 and 3 months of age. At the 16-month follow-up, the Gesell Developmental Schedule indicated a general developmental quotient of 93 with normal performance across all functional domains, demonstrating no psychomotor delay.

ObjectiveTo investigate the mechanism of action of Kaixinsan in the treatment of Alzheimer's disease （AD） based on network pharmacology， molecular docking， and animal experimental validation. MethodsThe Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（TCMSP） and the Encyclopedia of Traditional Chinese Medicine（ETCM） databases were used to obtain the active ingredients and targets of Kaixinsan. GeneCards， Online Mendelian Inheritance in Man（OMIM）， TTD， PharmGKB， and DrugBank databases were used to obtain the relevant targets of AD. The intersection （common targets） of the active ingredient targets of Kaixinsan and the relevant targets of AD was taken， and the network interaction analysis of the common targets was carried out in the STRING database to construct a protein-protein interaction（PPI） network. The CytoNCA plugin within Cytoscape was used to screen out the core targets， and the Metascape platform was used to perform gene ontology（GO） functional enrichment analysis and Kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment analysis. The “drug-active ingredient-target” interaction network was constructed with the help of Cytoscape 3.8.2， and AutoDock Vina was used for molecular docking. Scopolamine （SCOP） was utilized for modeling and injected intraperitoneally once daily. Thirty-two male C57/BL6 mice were randomly divided into blank control （CON） group （0.9% NaCl， n=8）， model （SCOP） group （3 mg·kg^-1·d^-1， n=8）， positive control group （3 mg·kg^-1·d^-1 of SCOP+3 mg·kg^-1·d^-1 of Donepezil， n=8）， and Kaixinsan group （3 mg·kg^-1·d^-1 of SCOP+6.5 g·kg^-1·d^-1 of Kaixinsan， n=8）. Mice in each group were administered with 0.9% NaCl， Kaixinsan， or Donepezil by gavage twice a day for 14 days. Morris water maze experiment was used to observe the learning memory ability of mice. Hematoxylin-eosin （HE） staining method was used to observe the pathological changes in the CA1 area of the mouse hippocampus. Enzyme linked immunosorbent assay（ELISA） was used to determine the serum acetylcholine （ACh） and acetylcholinesterase （AChE） contents of mice. Western blot method was used to detect the protein expression levels of signal transducer and activator of transcription 3（STAT3） and nuclear transcription factor（NF）-κB p65 in the hippocampus of mice. ResultsA total of 73 active ingredients of Kaixinsan were obtained， and 578 potential targets （common targets） of Kaixinsan for the treatment of AD were screened out. Key active ingredients included kaempferol， gijugliflozin， etc.. Potential core targets were STAT3， NF-κB p65， et al. GO functional enrichment analysis obtained 3 124 biological functions， 254 cellular building blocks， and 461 molecular functions. KEGG pathway enrichment obtained 248 pathways， mainly involving cancer-related pathways， TRP pathway， cyclic adenosine monophosphate（cAMP） pathway， and NF-κB pathway. Molecular docking showed that the binding of the key active ingredients to the target targets was more stable. Morris water maze experiment indicated that Kaixinsan could improve the learning memory ability of SCOP-induced mice. HE staining and ELISA results showed that Kaixinsan had an ameliorating effect on central nerve injury in mice. Western blot test indicated that Kaixinsan had a down-regulating effect on the levels of NF-κB p65 phosphorylation and STAT3 phosphorylation in the hippocampal tissue of mice in the SCOP model. ConclusionKaixinsan can improve the cognitive impairment function in SCOP model mice and may reduce hippocampal neuronal damage and thus play a therapeutic role in the treatment of AD by regulating NF-κB p65， STAT3， and other targets involved in the NF-κB signaling pathway.