ObjectiveTo investigate the effects and underlying mechanisms of Shenqi Wenfei prescription （SQWF） on chronic obstructive pulmonary disease （COPD）. MethodsA rat model of COPD with lung Qi deficiency was established using lipopolysaccharide （LPS） combined with cigarette smoke. Forty-eight SD rats were randomly divided into a blank group， a model group， low-， medium-， and high-dose SQWF groups （2.835， 5.67， 11.34 g·kg^-1）， and a Yupingfeng group （1.35 g·kg^-1）. Drug administration began on day 29 after modeling and continued for 2 weeks. The general condition of the rats was observed， and the lung function in each group was assessed. Hematoxylin-eosin （HE） staining was used to observe pathological changes in lung tissue. The proportion of inflammatory cells in bronchoalveolar lavage fluid （BALF） was measured. Apoptosis in lung tissue was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） staining. The release level of lactate dehydrogenase （LDH） in BALF was detected by a microplate assay. Reactive oxygen species （ROS） levels in lung tissue were detected using fluorescent probes. The levels of malondialdehyde （MDA）， total superoxide dismutase （SOD）， and reduced glutathione （GSH） in BALF were measured by biochemical methods. Ultrastructural changes in lung cells were observed via transmission electron microscopy. Double immunofluorescence staining was performed to detect the expression of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） in lung tissue. Western blot analysis was used to detect the protein expression of TXNIP， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific protease-1 （Caspase-1）， Caspase-1 p20， gasdermin D （GSDMD）， GSDMD N-terminal active fragment （GSDMD-N）， interleukin-1β （IL-1β）， and IL-18 in lung tissue. Serum IL-1β and IL-18 levels were measured by ELISA. ResultsCompared with the blank group， the model group showed lassitude， fatigue， tachypnea， and audible phlegm sounds， and lung function significantly declined （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were obvious. The level of inflammatory cells in BALF increased significantly （P0.05）. The number of TUNEL-positive cells increased （P0.01）. Levels of LDH， ROS， and MDA in BALF increased significantly （P0.01）， while GSH and SOD activities decreased significantly （P0.01）. Lung tissue cells showed irregular morphology， swollen mitochondria， disrupted cell membranes， and abundant vesicles， i.e.， pyroptotic bodies. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue were significantly elevated （P0.01）， and serum IL-1β and IL-18 levels also increased significantly （P0.01）. Compared with the model group， each medication group showed alleviation of qi deficiency symptoms and improved lung function （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were reduced. Inflammatory cell levels decreased （P0.05）. The number of TUNEL-positive cells decreased significantly （P0.01）. Levels of LDH， ROS， and MDA decreased significantly （P0.05）， while GSH and SOD activities significantly increased （P0.01）. Morphological and structural damage in lung tissue was improved to varying degrees. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue significantly decreased （P0.01）， and serum IL-1β and IL-18 levels also decreased significantly （P0.05）. ConclusionSQWF can improve lung function and alleviate inflammatory responses in COPD rats. Its mechanism may be related to regulating the ROS/TXNIP/NLRP3 pathway and inhibiting pyroptosis.

ObjectiveTo investigate the effects and underlying mechanisms of Shenqi Wenfei prescription （SQWF） on chronic obstructive pulmonary disease （COPD）. MethodsA rat model of COPD with lung Qi deficiency was established using lipopolysaccharide （LPS） combined with cigarette smoke. Forty-eight SD rats were randomly divided into a blank group， a model group， low-， medium-， and high-dose SQWF groups （2.835， 5.67， 11.34 g·kg^-1）， and a Yupingfeng group （1.35 g·kg^-1）. Drug administration began on day 29 after modeling and continued for 2 weeks. The general condition of the rats was observed， and the lung function in each group was assessed. Hematoxylin-eosin （HE） staining was used to observe pathological changes in lung tissue. The proportion of inflammatory cells in bronchoalveolar lavage fluid （BALF） was measured. Apoptosis in lung tissue was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） staining. The release level of lactate dehydrogenase （LDH） in BALF was detected by a microplate assay. Reactive oxygen species （ROS） levels in lung tissue were detected using fluorescent probes. The levels of malondialdehyde （MDA）， total superoxide dismutase （SOD）， and reduced glutathione （GSH） in BALF were measured by biochemical methods. Ultrastructural changes in lung cells were observed via transmission electron microscopy. Double immunofluorescence staining was performed to detect the expression of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） in lung tissue. Western blot analysis was used to detect the protein expression of TXNIP， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific protease-1 （Caspase-1）， Caspase-1 p20， gasdermin D （GSDMD）， GSDMD N-terminal active fragment （GSDMD-N）， interleukin-1β （IL-1β）， and IL-18 in lung tissue. Serum IL-1β and IL-18 levels were measured by ELISA. ResultsCompared with the blank group， the model group showed lassitude， fatigue， tachypnea， and audible phlegm sounds， and lung function significantly declined （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were obvious. The level of inflammatory cells in BALF increased significantly （P0.05）. The number of TUNEL-positive cells increased （P0.01）. Levels of LDH， ROS， and MDA in BALF increased significantly （P0.01）， while GSH and SOD activities decreased significantly （P0.01）. Lung tissue cells showed irregular morphology， swollen mitochondria， disrupted cell membranes， and abundant vesicles， i.e.， pyroptotic bodies. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue were significantly elevated （P0.01）， and serum IL-1β and IL-18 levels also increased significantly （P0.01）. Compared with the model group， each medication group showed alleviation of qi deficiency symptoms and improved lung function （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were reduced. Inflammatory cell levels decreased （P0.05）. The number of TUNEL-positive cells decreased significantly （P0.01）. Levels of LDH， ROS， and MDA decreased significantly （P0.05）， while GSH and SOD activities significantly increased （P0.01）. Morphological and structural damage in lung tissue was improved to varying degrees. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue significantly decreased （P0.01）， and serum IL-1β and IL-18 levels also decreased significantly （P0.05）. ConclusionSQWF can improve lung function and alleviate inflammatory responses in COPD rats. Its mechanism may be related to regulating the ROS/TXNIP/NLRP3 pathway and inhibiting pyroptosis.

ObjectiveThis paper aims to find the identified and validated clinical biomarker data building upon a clinical study of early-phase phase Ⅱ and investigate the correlation analysis of Huanglian Jiedu Wan on syndrome improvement and clinical biomarkers in the treatment of "excess heat-toxicity" based on a machine learning model. Additionally， the effective prediction of clinical biomarker values for the main symptoms of the "excess heat-toxicity" syndrome was assessed. MethodsA total of 229 patients meeting the inclusion criteria for "excess heat-toxicity" syndrome were randomly divided into the Huanglian Jiedu Wan group and the placebo group. Syndrome score transition matrices were constructed for the Huanglian Jiedu Wan group and the placebo group based on three main symptoms of "excess heat-toxicity" syndrome， such as oral ulcers， sore throat， and gum swelling and pain. Data from the patients with these three syndromes were also integrated for an overall analysis. The corresponding syndrome score transition matrices were further constructed to visualize symptom change trends of the patients in the two groups via heatmaps. Based on the identified and validated clinical biomarkers related to inflammation， oxidative stress， and energy metabolism in the early phase， Spearman correlation analysis was employed to analyze and evaluate the associations between clinical biomarkers and syndrome improvement. Key clinical biomarkers reflecting the effect of Huanglian Jiedu Wan were screened through the comparison of differences between groups. An extreme gradient boosting （XGBoost） algorithm was used to develop a prediction model for main symptom classification， with classification performance evaluated through 10-fold cross-validation. Feature importance analysis was applied to identify variables with the greatest contribution to the prediction result. ResultsThe syndrome transition matrix results indicated that the Huanglian Jiedu Wan group showed a superior effect to the placebo group in improving oral ulcers， sore throat， and overall symptoms， with significant effects observed especially in sore throat and overall symptom analyses （P<0.01）. Spearman correlation analysis revealed that several clinical biomarkers positively correlated with "excess heat-toxicity" syndrome and its main symptom improvement， were also called "heat-related biomarkers"， including succinic acid， α-ketoglutaric acid， glycine， lactic acid， adenosine monophosphate （AMP）， tumor necrosis factor-α （TNF-α）， interferon-γ （IFN-γ）， interleukin-1β （IL-1β）， interleukin-4 （IL-4）， interleukin-6 （IL-6）， interleukin-8 （IL-8）， interleukin-10 （IL-10）， and so on. Conversely， clinical biomarkers negatively correlated with symptom severity， were also called "heat-clearing related biomarkers" after administration of Huanglian Jiedu Wan， including malic acid， fumaric acid， cis-aconitic acid， adrenocorticotropic hormone （ACTH）， IL-1β， IL-4， IL-8， succinic acid， and citric acid. The XGBoost classification model using all 52 biomarkers as variables achieved an average test accuracy of 0.754 and an average F1 score of 0.777. Feature importance analysis identified the scores of glutamic acid in saliva and IL-6 were the highest in all the variables， with importance scores of 0.081 and 0.080， respectively. After screening out 14 key variables and optimizing the parameters， model performance improved to an average accuracy of 0.758 and an F1 score of 0.798. Feature importance analysis further determined that the glutamic acid in saliva and IL-6 showed obvious changes after screening the variables， confirming the good syndrome prediction ability of the model constructed by these key clinical biomarkers. ConclusionThis study systematically elucidates the correlation between syndrome improvement and clinical biomarkers of Huanglian Jiedu Wan in the treatment of "excess heat-toxicity" syndrome. An XGBoost classification model based on key clinical biomarkers is successfully established， achieving effective prediction of the symptoms related to the "excess heat-toxicity" syndrome such as oral ulcers and sore throat and providing a new insight for objective identification of traditional Chinese medicine syndromes.

ObjectiveThis paper aims to find the identified and validated clinical biomarker data building upon a clinical study of early-phase phase Ⅱ and investigate the correlation analysis of Huanglian Jiedu Wan on syndrome improvement and clinical biomarkers in the treatment of "excess heat-toxicity" based on a machine learning model. Additionally， the effective prediction of clinical biomarker values for the main symptoms of the "excess heat-toxicity" syndrome was assessed. MethodsA total of 229 patients meeting the inclusion criteria for "excess heat-toxicity" syndrome were randomly divided into the Huanglian Jiedu Wan group and the placebo group. Syndrome score transition matrices were constructed for the Huanglian Jiedu Wan group and the placebo group based on three main symptoms of "excess heat-toxicity" syndrome， such as oral ulcers， sore throat， and gum swelling and pain. Data from the patients with these three syndromes were also integrated for an overall analysis. The corresponding syndrome score transition matrices were further constructed to visualize symptom change trends of the patients in the two groups via heatmaps. Based on the identified and validated clinical biomarkers related to inflammation， oxidative stress， and energy metabolism in the early phase， Spearman correlation analysis was employed to analyze and evaluate the associations between clinical biomarkers and syndrome improvement. Key clinical biomarkers reflecting the effect of Huanglian Jiedu Wan were screened through the comparison of differences between groups. An extreme gradient boosting （XGBoost） algorithm was used to develop a prediction model for main symptom classification， with classification performance evaluated through 10-fold cross-validation. Feature importance analysis was applied to identify variables with the greatest contribution to the prediction result. ResultsThe syndrome transition matrix results indicated that the Huanglian Jiedu Wan group showed a superior effect to the placebo group in improving oral ulcers， sore throat， and overall symptoms， with significant effects observed especially in sore throat and overall symptom analyses （P<0.01）. Spearman correlation analysis revealed that several clinical biomarkers positively correlated with "excess heat-toxicity" syndrome and its main symptom improvement， were also called "heat-related biomarkers"， including succinic acid， α-ketoglutaric acid， glycine， lactic acid， adenosine monophosphate （AMP）， tumor necrosis factor-α （TNF-α）， interferon-γ （IFN-γ）， interleukin-1β （IL-1β）， interleukin-4 （IL-4）， interleukin-6 （IL-6）， interleukin-8 （IL-8）， interleukin-10 （IL-10）， and so on. Conversely， clinical biomarkers negatively correlated with symptom severity， were also called "heat-clearing related biomarkers" after administration of Huanglian Jiedu Wan， including malic acid， fumaric acid， cis-aconitic acid， adrenocorticotropic hormone （ACTH）， IL-1β， IL-4， IL-8， succinic acid， and citric acid. The XGBoost classification model using all 52 biomarkers as variables achieved an average test accuracy of 0.754 and an average F1 score of 0.777. Feature importance analysis identified the scores of glutamic acid in saliva and IL-6 were the highest in all the variables， with importance scores of 0.081 and 0.080， respectively. After screening out 14 key variables and optimizing the parameters， model performance improved to an average accuracy of 0.758 and an F1 score of 0.798. Feature importance analysis further determined that the glutamic acid in saliva and IL-6 showed obvious changes after screening the variables， confirming the good syndrome prediction ability of the model constructed by these key clinical biomarkers. ConclusionThis study systematically elucidates the correlation between syndrome improvement and clinical biomarkers of Huanglian Jiedu Wan in the treatment of "excess heat-toxicity" syndrome. An XGBoost classification model based on key clinical biomarkers is successfully established， achieving effective prediction of the symptoms related to the "excess heat-toxicity" syndrome such as oral ulcers and sore throat and providing a new insight for objective identification of traditional Chinese medicine syndromes.

Objective To construct a dynamic prediction model for JC polyomavirus (JCV) reactivation after kidney transplantation. Methods A retrospective analysis was conducted on the clinical data of 128 recipients who met the inclusion criteria and received kidney transplantation in Nanfang Hospital, Southern Medical University, from June 2021 to December 2024. Dynamic Cox regression and dynamic restricted mean survival time (RMST) regression based on the landmark method were adopted to establish the dynamic prediction models, and Monte Carlo cross-validation was used to evaluate model performance. Results The dynamic models could predict the incidence and onset time of JCV reactivation within the subsequent 3 months according to covariates at each landmark time point from the 1st to the 6th month after transplantation. Remuzzi score, body mass index and warm ischemia time were independent risk factors for JCV reactivation, while a history of urinary BK polyomavirus reactivation served as a protective factor. The median values of the area under the curve, C-index and Brier score of the dynamic Cox model were 0.873, 0.851 and 0.065 respectively, and the C-index of the dynamic RMST model was 0.829, all of which were superior to those of the static model. Conclusions The landmark-based dynamic models exhibit excellent predictive performance, which may integrate baseline data and post-transplant follow-up information to realize dynamic assessment of the risk and time window of JCV reactivation, thereby providing evidence for optimizing post-operative monitoring and individualized intervention strategies.

Objective:To investigate the current status of standardized residency training (SRT) teaching activities at Zhongshan Hospital affiliated to Fudan University, and to explore optimization strategies.Methods:We collected behavioral data from the SRT course selection platform and resident questionnaire survey data throughout 2024. Descriptive analysis, chi-square test, Mann-Whitney U test, and multivariable logistic regression analysis were performed. Results:A total of 170 teaching sessions were conducted in 2024, with interactive practice-based sessions accounting for 42.35% and lecture-based sessions accounting for 47.06%. According to 536 questionnaires, residents' overall satisfaction with teaching activities scored 87.83 points (high satisfaction, ≥85 points; moderate satisfaction, <85 points). The proportion of high satisfaction with interactive practice-based sessions was significantly higher than that with lecture-based sessions (82.81% vs. 75.46%, P=0.034). The enrollment for weekday evening courses filled up significantly faster than that for weekday daytime courses [4 (2, 6) seconds vs. 12 (8, 15) seconds, P<0.001]. Interactive practice-based sessions [odds ratio ( OR)=1.6, 95% CI=1.1-2.3, P=0.018] and weekday evening sessions ( OR=1.4, 95% CI=1.0-2.0, P=0.048) significantly improved resident satisfaction. Conclusions:Optimizing course formats and scheduling can enhance the quality of SRT teaching activities.

Transjugular intrahepatic portosystemic shunt(TIPS)is an important intervention for portal hypertension,and the degree of reduction in portal venous pressure is closely associated with the prognosis of patients.While a greater reduction in portal venous pressure may lead to more effective alleviation of portal hypertensive symptoms in cirrhotic patients,it also increases the risk of hepatic encephalopathy and liver failure.Therefore,appropriate control of the degree of reduction in portal venous pressure is essential for optimizing therapeutic outcomes.This article reviews the methods for measuring portal venous pressure,the factors affecting the reduction in portal venous pressure,the optimal range for reduction in different indications,and the impact of varying degrees of pressure reduction on complications,in order to provide guidance for improving the treatment outcome of TIPS and the prognosis of patients after surgery.

Objective:To investigate the effects of KH-type splicing regulatory protein(KHSRP)targeting and regulating JAK1/STAT3 signaling axis on the proliferation,migration and invasion of the adenocarcinoma of esophagogastric junction(AEG)cells,as well as the growth of transplanted tumors and lung metastasis.Methods:A total of 64 pairs of AEG tissue and adjacent normal tissue samples,along with clinical data from patients diagnosed at Huaihe Hospital from January 2017 to December 2018 were collected.The expression level of KHSRP in AEG tissues and adjacent normal tissues was observed using immunohistochemical staining.The differential expression of KHSRP in AEG cells(OE-19,TE-7,BIC-1,FLO-1,SK-GT-4,BE-3)and normal esophageal epithelial cells(Het-1A)was detected by qPCR.Lentiviral vectors were used to knockdown and overexpress KHSRP in OE-19,TE-7,FLO-1,and SK-GT-4 cells.The experiment was divided into the following groups:sh-NC group,sh-KHSRP group,Vector group,and KHSRP overexpression group(KHSRP group).The knockdown or overexpression efficiency was detected by qPCR,and the effects of KHSRP knockdown or overexpression on AEG cell proliferation,migration and invasion were evaluated using CCK-8 and Transwell assays,respectively.A mouse xenograft and lung metastasis model was established to observe the effects of KHSRP on tumor growth and metastasis in vivo.The targeted regulation of JAK/STAT signaling pathway by KHSRP was verified by Western blotting.A rescue experiment was conducted to verify whether KHSRP promoted malignant progression of AEG cells through the JAK1/STAT3 signaling pathway.Results:Compared with adjacent normal tissues,the expression level of KHSRP in AEG tissues was significantly increased(P<0.05 or P<0.01).Cell function experiments showed that KHSRP overexpression significantly promoted AEG cell proliferation,migration,and invasion in vitro(P<0.05 or P<0.01).In vivo animal experiments showed that KHSRP promoted AEG cell xenograft tumor growth and lung metastasis in nude mice(P<0.05 or P<0.01).After KHSRP knockdown,the phosphorylation levels of JAK1 and STAT3 in the JAK/STAT signaling pathway were significantly reduced,while overexpression of KHSRP led to the opposite results(P<0.05 or P<0.01).Rescue experiment showed that KHSRP could reverse the inhibition of cell proliferation,migration,and invasion caused by JAK1/STAT3 knockdown(P<0.05 or P<0.01).Conclusion:KHSRP regulates the malignant progression of AEG cells by activating JAK1/STAT3 signaling axis.KHSRP may become a potential target for the clinical treatment of AEG.

Objective To investigate the protective effect and mechanism of paeoniflorigenone(PFG),a natural active com-ponent in Xiongshao Capsule,against oxidized low-density lipoprotein(ox-LDL)induced vascular endothelial cell injury.Methods Network pharmacology and molecular docking were employed to identify hub targets and key active components of Xiongshao Capsulefor treating atherosclerosis.Human umbilicalvein endothelial cells(HUVECs)were divided into control,ox-LDL(100 μg/mL),PFG low-dose(20 μmol/L),and PFG high-dose(80 μmol/L)groups.Thecytotoxicity of PFG(10-160 μmol/L)and ox-LDL(5-200 μg/mL)was evaluated using the cell counting kit-8(CCK-8)assay.The effects of PFG(10,20,40,80 μmol/L)on ox-LDL-induced HUVEC viability after 24 hours of intervention were detected.Apoptosis was measured by flow cytome-try.The release of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1β(IL-1β)were quantified by enzyme-linked immunosorbent assay(ELISA).The mRNA expression levels of hub genes(EGFR,PIK3CA,SRC)were assessed by re-verse transcription quantitative PCR(qRT-PCR).Results Network pharmacology and molecular docking analysis demonstrated that PFG was a key active component of Xiongshao Capsule for treating atherosclerosis,stably binding to hub targets(EGFR,PIK3CA,and SRC)with binding affinities＜-7.0 kcal/mol.In vitro experiments revealed that compared to the control group,PFG-treated HUVECs showed no significant change in viability,while the ox-LDL group exhibited significantly reduced cell vi-ability,increased apoptosis levels,elevated concentrations of pro-inflammatory cytokines(TNF-α,IL-6,IL-1β),and upregulated mRNA expression of hub targets(EGFR,PIK3CA,SRC)(all P＜0.05).Compared to the ox-LDL group,PFG intervention sig-nificantly increased cell viability and decreased apoptosis levels,pro-inflammatory cytokine concentrations,and mRNA expres-sion of hub targets(all P＜0.05)in a dose-dependent manner.Conclusion This study demonstrates that PFG,the pivotal active ingredient of Xiongshao Capsule,may attenuate ox-LDL-induced vascular endothelial cell injury through the EGFR/PIK3CA/SRC regulatory axis.

Objective To investigate the protective effect and mechanism of paeoniflorigenone(PFG),a natural active com-ponent in Xiongshao Capsule,against oxidized low-density lipoprotein(ox-LDL)induced vascular endothelial cell injury.Methods Network pharmacology and molecular docking were employed to identify hub targets and key active components of Xiongshao Capsulefor treating atherosclerosis.Human umbilicalvein endothelial cells(HUVECs)were divided into control,ox-LDL(100 μg/mL),PFG low-dose(20 μmol/L),and PFG high-dose(80 μmol/L)groups.Thecytotoxicity of PFG(10-160 μmol/L)and ox-LDL(5-200 μg/mL)was evaluated using the cell counting kit-8(CCK-8)assay.The effects of PFG(10,20,40,80 μmol/L)on ox-LDL-induced HUVEC viability after 24 hours of intervention were detected.Apoptosis was measured by flow cytome-try.The release of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1β(IL-1β)were quantified by enzyme-linked immunosorbent assay(ELISA).The mRNA expression levels of hub genes(EGFR,PIK3CA,SRC)were assessed by re-verse transcription quantitative PCR(qRT-PCR).Results Network pharmacology and molecular docking analysis demonstrated that PFG was a key active component of Xiongshao Capsule for treating atherosclerosis,stably binding to hub targets(EGFR,PIK3CA,and SRC)with binding affinities＜-7.0 kcal/mol.In vitro experiments revealed that compared to the control group,PFG-treated HUVECs showed no significant change in viability,while the ox-LDL group exhibited significantly reduced cell vi-ability,increased apoptosis levels,elevated concentrations of pro-inflammatory cytokines(TNF-α,IL-6,IL-1β),and upregulated mRNA expression of hub targets(EGFR,PIK3CA,SRC)(all P＜0.05).Compared to the ox-LDL group,PFG intervention sig-nificantly increased cell viability and decreased apoptosis levels,pro-inflammatory cytokine concentrations,and mRNA expres-sion of hub targets(all P＜0.05)in a dose-dependent manner.Conclusion This study demonstrates that PFG,the pivotal active ingredient of Xiongshao Capsule,may attenuate ox-LDL-induced vascular endothelial cell injury through the EGFR/PIK3CA/SRC regulatory axis.