ObjectiveTo observe the effects of Dihuang Yinzi （DY） on motor dysfunction in rats with advanced Parkinson's disease （PD） and to investigate the mechanisms by which DY improves advanced PD symptoms through the "gut microbiota-short-chain fatty acids （SCFAs）-inflammation-neuroprotection pathway". MethodsAn advanced PD rat model was induced by rotenone. Rats were divided into a normal group， model group， positive drug group （levodopa， 50 mg·kg^-1）， and DY low-， medium-， and high-dose groups （5.2， 10.4， 20.8 g·kg^-1）. After 7 days of administration， motor function was evaluated using the open-field， pole-climbing， and inclined plate tests. Hematoxylin-eosin （HE） staining was used to observe pathological changes in the substantia nigra and colon， and immunohistochemistry was performed to detect α-Synuclein （α-Syn） and tyrosine hydroxylase （TH） expression in the substantia nigra. Enzyme-linked immunosorbent assay （ELISA） was used to measure levels of dopamine （DA）， 5-hydroxytryptamine （5-HT）， 3，4-dihydroxyphenylacetic acid （DOPAC）， Levodopa， homovanillic acid （HVA）， tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）. Western blot analysis was used to detect the expression of zonula occludens-1 （ZO-1） and occludin. Gut microbiota diversity was analyzed by 16S rRNA sequencing， and gas chromatography （GC） was used to determine the content of SCFAs in colonic contents. ResultsCompared with the normal group， the model group showed significantly decreased movement speed and distance in the open-field test， prolonged pole-climbing time， and reduced retention angle on the inclined plate （P<0.01）， accompanied by increased α-Syn expression （P<0.01） and decreased TH expression （P<0.01） in the brain. Compared with the model group， all DY dose groups improved motor dysfunction in advanced PD rats to varying degrees （P<0.05， P<0.01） and alleviated pathological damage in the brain and colon. High-dose DY significantly reduced α-Syn aggregation in the substantia nigra （P<0.01） and increased TH expression （P<0.01）. ELISA and Western blot results showed that， compared with the normal group， the model group exhibited decreased levels of DA， 5-HT， DOPAC， Levodopa， and HVA in the striatum （P<0.01）， increased levels of TNF-α， IL-6， and IL-1β in the colon and striatum （P<0.01）， and significantly reduced expression of ZO-1 （P<0.05） and occludin in the colon （P<0.01）. Compared with the model group， all DY dose groups increased the levels of DA， 5-HT， DOPAC， Levodopa， and HVA in the striatum to varying degrees （P<0.05， P<0.01）. In the high-dose DY group， the levels of TNF-α， IL-6， and IL-1β in the colon and striatum were reduced （P<0.01）， while the expression of ZO-1 （P<0.05） and occludin in the intestine was increased. The 16S rRNA sequencing results indicated that the relative abundances of Actinobacteriota， Enterobacteriaceae， and Erysipelotrichaceae were increased in the model group， whereas the relative abundances of Bacteroidota， class Clostridia， Lachnospiraceae， and Akkermansia muciniphila were decreased. These changes were effectively reversed after high-dose DY intervention. GC analysis showed that the content of SCFAs in the colonic contents of rats in the model group was decreased （P<0.05， P<0.01）， while after high-dose DY intervention， the levels of acetate， propionate， isobutyrate， and butyrate were significantly increased （P<0.05， P<0.01）. ConclusionDY may exert therapeutic effects in advanced PD by regulating the gut microbiota-SCFAs-inflammation pathway.

ObjectiveTo investigate the mechanisms by which Liuwei Buqi prescription （LWBQ） regulates alveolar macrophage efferocytosis and improves inflammatory responses in rats with chronic obstructive pulmonary disease （COPD） characterized by lung-kidney Qi deficiency based on the nuclear factor erythroid 2-related factor 2 （Nrf2）/macrophage receptor with collagenous structure （MARCO） pathway. MethodsSuccessfully modeled rats were randomly divided into a model group， low-dose LWBQ group （LWBQ-L， 2.25 g·kg^-1·d^-1）， medium-dose LWBQ group （LWBQ-M， 4.5 g·kg^-1·d^-1）， high-dose LWBQ group （LWBQ-H， 9 g·kg^-1·d^-1）， and aminophylline group （AMIN， 50 mg·kg^-1·d^-1）， with 8 rats in each group. Another 8 healthy rats were included as the blank group. Except for the blank group， rats in the remaining groups were subjected to smoke exposure combined with forced swimming， intratracheal lipopolysaccharide （LPS） instillation， and subcutaneous hydrocortisone injection to establish a COPD model with lung-kidney Qi deficiency. After successful modeling， rats were administered different doses of LWBQ or AMIN by gavage. Body weight， fur condition， and oral secretions were observed. Pulmonary function was measured using an animal lung function analyzer. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression levels of interferon-γ （IFN-γ）， interleukin-6 （IL-6）， interleukin-1 （IL-1）， and tumor necrosis factor-α （TNF-α） in bronchoalveolar lavage fluid （BALF） and serum （SER）. Hematoxylin-eosin （HE） staining was used to examine pathological changes in lung tissue. Giemsa staining was performed to detect eosinophils， basophils， and neutrophils in BALF. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） was used to detect apoptosis in lung tissue. Western blot and real-time polymerase chain reaction （Real-time PCR） were employed to determine the protein and mRNA expression levels of efferocytosis-related proteins growth arrest-specific gene 6 （GAS6）， milk fat globule-epidermal growth factor 8 （MFG-E8）， and pathway-related proteins Nrf2 and MARCO in lung tissue. ResultsCompared with the blank group， the model group showed reduced food intake， nasal and oral secretions with sputum， and decreased body weight （P<0.01）， decreased peak expiratory flow （PEF） （P<0.01）， increased forced vital capacity （FVC） （P<0.01）， and decreased forced expiratory volume in 0.3 s/forced vital capacity ［FEV0.3/FVC （%）］ （P<0.01）. The expression levels of IFN-γ， IL-6， IL-1， and TNF-α in BALF and SER were increased （P<0.01）. Lung tissue exhibited structural destruction， hyperplasia， inflammatory exudation， increased apoptotic cells， and increased mean optical density （P<0.01）. The protein and mRNA expression levels of GAS6， MFG-E8， and MARCO， as well as Nrf2 mRNA expression， were increased （P<0.01）. Compared with the model group， the LWBQ groups showed increased food intake， reduced nasal and oral secretions with sputum， and increased body weight （P<0.05， P<0.01）. PEF was increased （P<0.01）. FVC was increased in rats treated with low- and medium-dose LWBQ （P<0.01）， and FEV0.3/FVC （%） was increased in rats treated with medium- and high-dose LWBQ （P<0.05， P<0.01）. The expression levels of IFN-γ， IL-6， IL-1， and TNF-α in BALF and SER were decreased （P<0.01）. Lung tissue structure was relatively intact， with improvement in hyperplasia and inflammatory exudation. The number of apoptotic cells in lung tissue was reduced， and mean optical density was decreased （P<0.05， P<0.01）. The protein and mRNA expression levels of efferocytosis-related proteins GAS6 and MFG-E8 and pathway-related proteins Nrf2 and MARCO were increased （P<0.01）. ConclusionLWBQ can alleviate pulmonary and systemic inflammation， improve lung function， and reduce lung tissue damage in rats with COPD characterized by lung-kidney Qi deficiency. The mechanism may be related to enhancement of alveolar macrophage efferocytosis through regulation of the Nrf2/MARCO pathway.

The theory of constitution in traditional Chinese medicine （TCM） has emerged as a new discipline in recent years. Constitution plays a vital role in the onset，progression，transformation，and prognosis of diseases. At present，some clinical scholars have adopted a novel diagnostic and treatment model of "constitution differentiation-disease identification-syndrome differentiation"，in which constitution is regarded as a core element throughout the diagnostic and therapeutic process. Constitution is closely associated with etiology，onset，pathogenesis，syndrome differentiation，and treatment. Against this background，the construction of animal models based on constitution holds far-reaching significance for advancing clinical research. This paper focuses on the construction and evaluation of rodent models with Qi-deficiency constitution，aiming to explore how to further induce Qi-deficiency syndromes and related disease states on the basis of Qi-deficiency constitution models，thereby developing an integrated animal model that embodies the trinity of "constitution-disease-syndrome". The establishment of this model not only provides a solid experimental foundation for the development of new therapies and drugs in TCM targeting specific constitutions，diseases，and syndromes，but also greatly promotes the modernization and scientific advancement of TCM theory. By comprehensively applying multidisciplinary technologies and methods，the study evaluates the model's validity，reliability，and practicality，with the aim of opening new avenues for future research in TCM and promoting the development of the field.

The theory of constitution in traditional Chinese medicine （TCM） has emerged as a new discipline in recent years. Constitution plays a vital role in the onset，progression，transformation，and prognosis of diseases. At present，some clinical scholars have adopted a novel diagnostic and treatment model of "constitution differentiation-disease identification-syndrome differentiation"，in which constitution is regarded as a core element throughout the diagnostic and therapeutic process. Constitution is closely associated with etiology，onset，pathogenesis，syndrome differentiation，and treatment. Against this background，the construction of animal models based on constitution holds far-reaching significance for advancing clinical research. This paper focuses on the construction and evaluation of rodent models with Qi-deficiency constitution，aiming to explore how to further induce Qi-deficiency syndromes and related disease states on the basis of Qi-deficiency constitution models，thereby developing an integrated animal model that embodies the trinity of "constitution-disease-syndrome". The establishment of this model not only provides a solid experimental foundation for the development of new therapies and drugs in TCM targeting specific constitutions，diseases，and syndromes，but also greatly promotes the modernization and scientific advancement of TCM theory. By comprehensively applying multidisciplinary technologies and methods，the study evaluates the model's validity，reliability，and practicality，with the aim of opening new avenues for future research in TCM and promoting the development of the field.

Objective To propose a lightweight end-to-end neural network model for automated Korotkoff sound phase recognition and subsequent blood pressure (BP) measurement, aiming to improve measurement accuracy and population adaptability. Methods We developed a streamlined architecture integrating depthwise separable convolution (DSConv), multi-head attention (MHA), and bidirectional gated recurrent unit (BiGRU). The model directly processes Korotkoff sound time-series signals to identify auscultatory phases. Systolic BP (SBP) and diastolic BP (DBP) were determined using phase Ⅰ and phaseⅤdetections, respectively. Given the clinical relevance of phase Ⅳ for specific populations (e.g., children and pregnant women, denoted as DBPⅣ), BP values from this phase were also recorded.Results The study enrolled 106 volunteers with 70 males and 36 females at mean age of (40.0±12.0) years. The model achieved 94.25% phase recognition accuracy. Measurement errors were (0.1±2.5) mm Hg (SBP), (0.9±3.4) mm Hg (DBPⅣ), and (0.8±2.6) mm Hg (DBP). Conclusion Our method enables precise phase recognition and BP measurement, demonstrating potential for developing population-adaptive blood pressure monitoring systems.

Objective To explore the factors affecting the quality of psychological assistance hotline connections in Shaanxi Province, and to provide a basis for optimizing services. Methods A total of 149 calls with suicidal tendencies were included from January to March 2022, and data were collected by 31 trained assessors through standardized questionnaires (general information, suicide risk, emotional intensity, and wiring characteristics). Results The results showed that 56.38% of the callers were female, with age groups concentrated between ≤ 18 years old (29.53%) and 19-34 years old (43.62%). The call duration was mainly between 31 and 45 minutes (50.34%). Operators conducted a suicide risk assessment on the callers, with 38.9% having a comprehensive assessment, 38.9% having an incomplete assessment, and 22.1% having no assessment. The main mental disorders of the callers were depression (48.32%), anxiety (15.44%), and bipolar disorder (14.77%), with 25.50% having comorbidities of ≥ 2 disorders. Emotional scores were as follows: depression (4.11 ± 0.76), sadness (3.97 ± 1.03), and despair (3.78 ± 1.05). There were significant differences in depression, anger, despair, and sadness among the callers with different levels of danger (t=4.79, 3.35, 15.79, 4.24, all P<0.05). Women had higher levels of fear than men (t=3.10, P<0.01). The longer the call duration, the higher the level of despair (t=5.66, P<0.01). Multiple regression analysis showed that incomplete suicide risk assessment by operators (B=-2.36), general procedures for operators' connections (B=5.44), and technical factors (B=2.01) significantly affected the quality of psychological assistance hotlines (all P<0.05). Conclusion Callers with suicidal tendencies generally have serious mental and psychological problems and prominent negative emotions. Strengthening the suicide risk assessment ability of operators and standardizing processes and service attitudes are key to improving the quality of psychological assistance hotlines.

ObjectiveTo explore the effect and mechanism of Taishan Panshi powder （TSPSP） on inhibiting oxidative stress injury in human chorionic trophoblast cells （HTR-8/SVneo）， and to uelucidate the underlying mechanism of TSPSP in the treatment of spontaneous abortion （SA）. MethodsGene differential analysis of SA was performed using the Gene Expression Omnibus （GEO） database and correlated with oxidative stress. Network pharmacology was employed to screen the active components of TSPSP， and a "Chinese medicine-component-target-disease" network was constructed to predict the mechanism of action of TSPSP. For in vitro validation experiments， HTR-8/SVneo cells were divided into blank group， model group， TSPSP-containing serum 2.5%， 5%， 10% groups， and nuclear factor E₂-related factor 2 （Nrf2） inhibitor group （ML385， 30 μmol·L^-1）. Except for the blank group， other groups were stimulated with 150 μmol·L^-1 H₂O₂ for 3 h to establish a cell oxidative stress injury model. After successful modeling， the blank group and model group were given 10% blank serum， each TSPSP-containing serum group was treated with the corresponding concentration of drug-containing serum， and the Nrf2 inhibitor group was additionally given 30 μmol·L^-1 ML385 on the basis of 10% TSPSP-containing serum. All groups of cells were continuously cultured under the above conditions for 24 h， and then samples were collected for subsequent detection. Cell viability in each group was detected by CCK-8 assay. Cell migration rate was detected by scratch test. The contents of malondialdehyde （MDA）， Fe²⁺， and Glutathione （GSH） were detected by enzyme-linked immunosorbent assay （ELISA）. Intracellular reactive oxygen species （ROS） level was detected by a fluorescent probe （DCF-DA）. The protein and mRNA expression levels of Kelch-like ECH-associated protein 1 （KEAP1）， Nrf2， and forkhead box protein O3 （FoxO3） in cells were detected by immunofluorescence （IF） and real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression levels of KEAP1， Nrf2， FoxO3， Glutathione peroxidase 4 （GPX4）， and superoxide dismutase （SOD） in cells were detected by Western blot. ResultsThe GSE76862 and GSE22490 datasets were obtained from the GEO database. Differential gene analyses showed that the KEAP1， Nrf2， and FoxO3 genes were all associated with the disease. After matching with the oxidative stress pathway， nine significantly differential pathways were identified （P<0.05）， among which three contained the target genes Nrf2 and FoxO3. A total of 246 active ingredient targets of TSPSP and 2 804 SA-related targets were obtained through network pharmacology， and 154 potential action targets were obtained after taking the intersection. Topological analysis showed that targets such as KEAP1 and Nrf2 exhibited high degree values. GO and KEGG enrichment analyses indicated that the intersection targets were mainly involved in oxidative stress response， FOXO and MAPK signaling pathways， etc. In in vitro experiments， compared with the blank group， the cell viability in the model group was significantly decreased （P<0.01）. Compared with the model group， the cell viability in each TSPSP-containing serum group was significantly increased （P<0.01）. Compared with the 10% TSPSP-containing serum group， the cell viability in the ML385 group decreased to approximately 70% （P<0.01）. Compared with the blank group， the model group showed significantly increased contents of MDA， Fe²⁺， and ROS， decreased GSH expression （P<0.01）， significantly reduced cell migration rate （P<0.01）， and increased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.01）， while decreased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.01）. Compared with the model group， each TSPSP-containing serum group showed significantly decreased contents of MDA， Fe²⁺， and ROS， increased GSH expression （P<0.01）， significantly increased migration rate （P<0.01）， significantly decreased protein and mRNA expression levels of KEAP1 and FoxO3 （P<0.05， P<0.01）， and significantly increased protein and mRNA expression levels of Nrf2， GPX4， and SOD （P<0.05， P<0.01）. Compared with the 10% TSPSP-containing serum group， the ML385 group showed reversed trends in all indicators （P<0.05， P<0.01）. ConclusionTSPSP can inhibit H₂O₂-induced oxidative stress injury of trophoblast cells， and its mechanism of action may be related to the drug activating the KEAP1/Nrf2/FoxO3 signaling pathway.

ObjectiveTo investigate the molecular mechanisms by which salvianolic acid B （SalB） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） by downregulating phosphoribosylaminoimidazole carboxylase and phosphoribosylaminoimidazole succinocarboxamide synthetase （PAICS） expression. MethodsNSCLC A549 cells and normal bronchial epithelial cells （bronchial epithelium transformed with Ad12-SV40 2B， BEAS-2B） were used as models. Cell viability was assessed using the cell counting kit-8 （CCK-8） assay after treatment with SalB （0， 50， 100， 200， 300， 400， 500 μmol·L^-1 for 24 or 48 h to determine effective and safe intervention concentrations. Cell proliferation， cell cycle distribution， and apoptosis were evaluated by 5-ethynyl-2′-deoxyuridine （EdU） staining and flow cytometry， respectively. Wound healing and Transwell invasion assays were performed to assess cell migration and invasion. RNA sequencing combined with bioinformatic analysis was conducted to identify differentially expressed genes and functional enrichment. Molecular docking was used to predict the binding ability between SalB and PAICS， and the cellular thermal shift assay （CETSA） was performed to evaluate the effect of SalB on the thermal stability of the PAICS protein. Western blot （WB） was used to detect the effects of SalB on PAICS and EMT-related proteins （E-cadherin， N-cadherin， Vimentin， Snail， and Slug）. A functional rescue assay was conducted by PAICS overexpression via plasmid transfection. ResultsCompared with the control group， SalB inhibited A549 cell viability in a dose-dependent manner （P<0.05）， and the effective concentrations （≤300 μmol·L^-1） showed no significant cytotoxicity in BEAS-2B cells. Within this concentration range， SalB significantly inhibited A549 cell proliferation， migration， and invasion， and induced G₀/G₁ phase arrest and apoptosis （P<0.05）. Transcriptomic analysis showed that SalB significantly downregulated PAICS expression， and its functions were enriched in cell proliferation and EMT. Bioinformatic analysis indicated that PAICS is highly expressed in lung adenocarcinoma and is associated with poor prognosis （P<0.01）. Molecular docking showed that SalB has strong binding ability to PAICS （binding energy -9.1 kcal·mol^-1. CETSA results showed that SalB significantly increased the thermal stability of the PAICS protein （P<0.05）. WB results showed that， compared with the control group， SalB dose-dependently downregulated PAICS expression， upregulated E-cadherin， and downregulated N-cadherin， Vimentin， Snail， and Slug （P<0.05）. Functional rescue experiments showed that， compared with the empty vector group， PAICS overexpression significantly enhanced A549 cell proliferation， migration， and invasion， promoted cell cycle progression， and inhibited apoptosis （P<0.05）. Meanwhile， compared with the empty vector + SalB-H group， PAICS overexpression partially reversed the inhibitory effects of SalB on malignant phenotypes and EMT-related proteins （N-cadherin， Vimentin， Snail， and Slug）， and downregulated E-cadherin expression （P<0.05，P<0.01）， indicating that PAICS is a key functional target mediating the antitumor effects of SalB. ConclusionSalB effectively inhibits EMT progression and cell cycle progression in A549 cells by downregulating PAICS expression， thereby exerting anti-NSCLC effects. This study not only reveals that PAICS is a key functional target through which SalB regulates EMT， but also provides experimental evidence supporting SalB as a potential candidate drug for inhibiting NSCLC metastasis.

ObjectiveTo investigate the inhibitory effects of curcumol （Cur） on the proliferation and metastasis of non-small cell lung cancer （NSCLC） cells and to explore the underlying mechanisms. MethodsIn vivo， a subcutaneous tumor xenograft model was established to evaluate the antiproliferative effect of Cur. In vitro， the cell counting kit-8 （CCK-8） assay was used to assess the effects of Cur at concentrations of 0， 60， 120， 240， 360， 480， 600， 720， 840， 960 μmol·L^-1 on the viability of NCI-A549 and NCI-H23 cells， and to evaluate its inhibitory effect on the proliferation of human bronchial epithelial BEAS-2B cells. Wound healing and Transwell migration assays were conducted to assess changes in cell migratory capacity following Cur treatment. Immunohistochemistry （IHC-P） was used to investigate the regulatory effect of Cur on the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway in tumor tissues. Western blot was performed to determine the protein expression levels of phosphorylated JAK2 （p-JAK2）， phosphorylated STAT3 （p-STAT3）， proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） in tumor tissues and cells. To further verify the role of the JAK2/STAT3 signaling pathway in the pharmacological effects of Cur， rescue experiments were performed using the pathway agonist colivelin. ResultsIn vivo experiments showed that， compared with the model group， the tumor volumes of subcutaneous xenografts in nude mice in both low- and high-dose Cur groups were significantly reduced （P<0.05）， and the tumor inhibition rates were significantly increased （P<0.05）. The inhibitory effect in the high-dose group was comparable to that of the cisplatin group， and the body weight of mice in the Cur groups remained stable throughout the experiment. In vitro， compared with the control group， Cur at concentrations of 120 and 240 μmol·L^-1 inhibited the proliferation of NCI-A549 and NCI-H23 cells in a concentration-dependent manner （P<0.05）， with a significant inhibitory effect observed at 360 μmol·L^-1 （P<0.01）， while no significant effect on the viability of BEAS-2B cells was observed. Migration assays demonstrated that， compared with the control group， Cur treatment significantly reduced the migration rates of both cell lines in a concentration-dependent manner （P<0.05）， with an inhibitory effect at 360 μmol·L^-1 comparable to that of the cisplatin group. Mechanistic validation showed that， compared with the control group， the protein expression levels of p-JAK2 and p-STAT3 in tumor tissues and cells were significantly downregulated in the Cur groups （P<0.01）， and the expression levels of downstream proteins PCNA， MMP-2， MMP-9， and VEGFA were also significantly decreased with increasing Cur concentration （P<0.05）. In the rescue experiments， compared with the control group， colivelin pretreatment increased cell proliferation and migration rates （P<0.05） and upregulated the expression of related proteins （P<0.05）. Compared with the Cur group， the colivelin+Cur group showed significantly increased proliferation and migration rates （P<0.05）， along with significantly upregulated protein expression levels （P<0.05）. ConclusionCur can significantly inhibit the proliferation and metastasis of NSCLC both in vivo and in vitro， and its mechanism of action is closely associated with the inhibition of JAK2/STAT3 signaling pathway activation.

ObjectiveTo investigate the mechanisms by which oxyresveratrol （OXY） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） through the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsCell counting kit-8 （CCK-8） assays were used to determine the survival rates of A549 and H1299 cells treated with different concentrations of OXY， and appropriate concentrations （0， 30， 60， 90 μmol·L^-1） were selected. The effects of OXY on the proliferation of A549 and H1299 cells were evaluated using 5-ethynyl-2′-deoxyuridine （EdU） assays and colony formation assays. Wound healing assays and Transwell invasion assays were performed to assess the effects of OXY on cell migration and invasion. Western blot （WB） was used to detect the expression levels of Snail， E-cadherin， N-cadherin， and Vimentin in A549 and H1299 cells. Network pharmacology and molecular docking were applied to predict the mechanism of action of OXY， and WB was used to evaluate the effects of OXY on proteins in the PI3K/Akt signaling pathway. Rescue experiments were conducted using the PI3K/Akt signaling pathway agonist 740Y-P. Under activation of the PI3K/Akt pathway， the effect of OXY on proliferation， migration， and invasion phenotypes， as well as on the expression levels of PI3K/Akt pathway-related proteins and EMT markers （Snail， E-cadherin， N-cadherin， and Vimentin）， were examined. ResultsIn the forward experiments， CCK-8 assay results showed that， compared with the control group， the survival rates of NSCLC cells in the OXY-treated groups （20-120 μmol·L^-1） were significantly decreased （P<0.05）. The half-maximal inhibitory concentration （IC₅₀） values of A549 and H1299 cells after 48 h of OXY treatment were 113.6 μmol·L^-1 and 92.53 μmol·L^-1， respectively. Therefore， concentrations of 0， 30， 60， 90 μmol·L^-1 were selected as the gradient for subsequent phenotypic and mechanistic studies. Compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the OXY groups （30， 60， and 90 μmol·L^-1） were significantly decreased （P<0.01， P<0.05）. WB results showed that， compared with the control group， the protein expression levels of Snail， N-cadherin， and Vimentin in NSCLC cells of the OXY groups were significantly decreased （P<0.05）， whereas E-cadherin expression was significantly increased （P<0.01）. Network pharmacology and molecular docking results indicated that OXY could act on the PI3K/Akt signaling pathway and exhibited good binding affinity with PI3K and Akt proteins. Further WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in NSCLC cells of the OXY groups， whereas the expression levels of phosphorylated PI3K （p-PI3K） and phosphorylated Akt （p-Akt） were significantly decreased （P<0.05）. In the rescue experiments， compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the 740Y-P group （15 μmol·L^-1） were significantly increased （P<0.01）. Compared with the control + OXY group （90 μmol·L^-1）， these indices in the 740Y-P + OXY group （15 μmol·L^-1 + 90 μmol·L^-1） were also significantly increased （P<0.01）. WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in the 740Y-P group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.01）. Compared with the control + OXY group， there were no statistically significant differences in PI3K and Akt protein expression in the 740Y-P + OXY group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.05）. ConclusionOXY inhibits the PI3K/Akt signaling pathway and suppresses the EMT process， thereby exerting anti-metastatic effects in NSCLC.