ObjectiveThis paper aims to explore the in vitro anti-psoriasis activity and potential mechanism of Kangfuxin liquid （KFX liquid）， providing experimental evidence for the anti-psoriasis effect of KFX liquid. MethodsFirstly， the uninduced human immortalized keratinocyte cells （HaCaT cells） were divided into seven groups， namely the control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. After being treated with different concentrations of KFX liquid， the effect of KFX liquid on the normal cell proliferation was detected by using the cell counting kit-8 （CCK-8） method. Secondly， the uninduced HaCaT cells were divided into six groups， namely the control group and recombinant human interleukin-7A （rh-IL-7A） groups with different doses （5， 10， 50， 100， 120 g·L^-1）. After being treated with different concentrations of recombinant human interleukin-17A （rh IL-17A） liquid， the effect of rh IL-17A on cell proliferation was detected. The optimal induction concentration was screened. Then， normal HaCaT cells were divided into a control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. Except for the control group， the other groups established psoriasis cell models with the optimal induction concentration of rh IL-17A. After being treated with different concentrations of KFX liquid， the effects of KFX liquid on the psoriasis-like HaCaT cell proliferation were investigated. Finally， the uninduced HaCaT cells were divided into six groups， namely the control group， rh IL-17A group， methotrexate （MTX） group， and KFX liquid groups with different doses （20， 40， 80 g·L^-1）. Except for the control group， the other groups used the optimal induction concentration of rh IL-17A to establish psoriasis cell models. After being treated with different drugs， the cell migration levels were detected through scratch assays， and real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the relative mRNA expression levels of Ki-67 antigen （Ki67）， S100 calcium-binding protein A7 （S100A7）， S100 calcium-binding protein A8 （S100A8）， and S100 calcium-binding protein A9 （S100A9）， thereby comprehensively evaluating the in vitro anti-psoriasis activity of KFX liquid. By detecting the relative mRNA expression levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and chemokine-20 （CXCL-20） inflammatory-related factors in psoriasis-like HaCaT cells and the protein expression levels of Janus kinase 3 （JAK3）， phosphorylated Janus kinase 3 （p-JAK3）， signal transducer and activator of transcription 3 （STAT3）， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）， the mechanism was explored. ResultsCompared with that of control group， when treated with 80 g·L^-1 KFX liquid for 72 h （P<0.05） and at different times with 160 g·L^-1 KFX liquid， the HaCaT cell proliferation activity was significantly affected （P<0.01）， while the other concentrations of KFX liquid had no significant differences in cell morphology and cell proliferation activity at different times， indicating that the KFX liquid is relatively safe for HaCaT cells and has no obvious toxic side effects. Compared with that of control group， when treated with different concentrations of rh IL-17A for 24 h， the HaCaT cell proliferation activity was significantly enhanced， and the cell activity was the strongest when the concentration was 100 μg·L^-1 （P<0.05）， with a density close to 100% and intact cell morphology， indicating that 100 μg·L^-1 is the optimal concentration for inducing HaCaT cell proliferation. The results of the KFX liquid treatment on rh IL-17A-induced psoriasis-like cells show that the KFX liquid not only effectively inhibits the rh IL-17A-induced psoriasis-like HaCaT cell proliferation activity （P<0.01）， but also significantly reduces the migration ability of rh IL-17A-induced psoriasis-like HaCaT cells （P<0.01）， and the relative mRNA expression levels of Ki67， S100A7， S100A8， and S100A9 （P<0.01）. Moreover， the KFX liquid can significantly reduce the relative mRNA expression levels of IL-1β， IL-6， and CXCL-20 in rh IL-17A-induced psoriasis-like cells （P<0.01）， and significantly inhibit the phosphorylation levels of JAK3 and STAT3 proteins （P<0.05， P<0.01）. ConclusionThe KFX liquid has no obvious toxicity to uninduced HaCaT cells. It can inhibit rh IL-17A-induced psoriasis-like HaCaT cell proliferation， reduce the cell migration ability， and has good in vitro anti-psoriasis activity. Its action mechanism may be related to downregulating the expression levels of inflammation-related cytokines in the JAK3/STAT3 signaling pathway and inhibiting the phosphorylation levels of JAK3 and STAT3 proteins.

ObjectiveThis paper aims to explore the in vitro anti-psoriasis activity and potential mechanism of Kangfuxin liquid （KFX liquid）， providing experimental evidence for the anti-psoriasis effect of KFX liquid. MethodsFirstly， the uninduced human immortalized keratinocyte cells （HaCaT cells） were divided into seven groups， namely the control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. After being treated with different concentrations of KFX liquid， the effect of KFX liquid on the normal cell proliferation was detected by using the cell counting kit-8 （CCK-8） method. Secondly， the uninduced HaCaT cells were divided into six groups， namely the control group and recombinant human interleukin-7A （rh-IL-7A） groups with different doses （5， 10， 50， 100， 120 g·L^-1）. After being treated with different concentrations of recombinant human interleukin-17A （rh IL-17A） liquid， the effect of rh IL-17A on cell proliferation was detected. The optimal induction concentration was screened. Then， normal HaCaT cells were divided into a control group and KFX liquid groups with different doses （5， 10， 20， 40， 80， 160 g·L^-1）. Except for the control group， the other groups established psoriasis cell models with the optimal induction concentration of rh IL-17A. After being treated with different concentrations of KFX liquid， the effects of KFX liquid on the psoriasis-like HaCaT cell proliferation were investigated. Finally， the uninduced HaCaT cells were divided into six groups， namely the control group， rh IL-17A group， methotrexate （MTX） group， and KFX liquid groups with different doses （20， 40， 80 g·L^-1）. Except for the control group， the other groups used the optimal induction concentration of rh IL-17A to establish psoriasis cell models. After being treated with different drugs， the cell migration levels were detected through scratch assays， and real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the relative mRNA expression levels of Ki-67 antigen （Ki67）， S100 calcium-binding protein A7 （S100A7）， S100 calcium-binding protein A8 （S100A8）， and S100 calcium-binding protein A9 （S100A9）， thereby comprehensively evaluating the in vitro anti-psoriasis activity of KFX liquid. By detecting the relative mRNA expression levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and chemokine-20 （CXCL-20） inflammatory-related factors in psoriasis-like HaCaT cells and the protein expression levels of Janus kinase 3 （JAK3）， phosphorylated Janus kinase 3 （p-JAK3）， signal transducer and activator of transcription 3 （STAT3）， and phosphorylated signal transducer and activator of transcription 3 （p-STAT3）， the mechanism was explored. ResultsCompared with that of control group， when treated with 80 g·L^-1 KFX liquid for 72 h （P<0.05） and at different times with 160 g·L^-1 KFX liquid， the HaCaT cell proliferation activity was significantly affected （P<0.01）， while the other concentrations of KFX liquid had no significant differences in cell morphology and cell proliferation activity at different times， indicating that the KFX liquid is relatively safe for HaCaT cells and has no obvious toxic side effects. Compared with that of control group， when treated with different concentrations of rh IL-17A for 24 h， the HaCaT cell proliferation activity was significantly enhanced， and the cell activity was the strongest when the concentration was 100 μg·L^-1 （P<0.05）， with a density close to 100% and intact cell morphology， indicating that 100 μg·L^-1 is the optimal concentration for inducing HaCaT cell proliferation. The results of the KFX liquid treatment on rh IL-17A-induced psoriasis-like cells show that the KFX liquid not only effectively inhibits the rh IL-17A-induced psoriasis-like HaCaT cell proliferation activity （P<0.01）， but also significantly reduces the migration ability of rh IL-17A-induced psoriasis-like HaCaT cells （P<0.01）， and the relative mRNA expression levels of Ki67， S100A7， S100A8， and S100A9 （P<0.01）. Moreover， the KFX liquid can significantly reduce the relative mRNA expression levels of IL-1β， IL-6， and CXCL-20 in rh IL-17A-induced psoriasis-like cells （P<0.01）， and significantly inhibit the phosphorylation levels of JAK3 and STAT3 proteins （P<0.05， P<0.01）. ConclusionThe KFX liquid has no obvious toxicity to uninduced HaCaT cells. It can inhibit rh IL-17A-induced psoriasis-like HaCaT cell proliferation， reduce the cell migration ability， and has good in vitro anti-psoriasis activity. Its action mechanism may be related to downregulating the expression levels of inflammation-related cytokines in the JAK3/STAT3 signaling pathway and inhibiting the phosphorylation levels of JAK3 and STAT3 proteins.

Jiuwei Xifeng Granules have become a Chinese patent medicine in the market. Because the formula contains Os Draconis, a top-level protected fossil of ancient organisms, the formula was to be improved by replacing Os Draconis with Ostreae Concha. To evaluate whether the improved formula has the same effectiveness and safety as the original formula, a randomized, double-blind, parallel-controlled, equivalence clinical trial was conducted. This study enrolled 288 tic disorder(TD) of children and assigned them into two groups in 1∶1. The treatment group and control group took the modified formula and original formula, respectively. The treatment lasted for 6 weeks, and follow-up visits were conducted at weeks 2, 4, and 6. The primary efficacy endpoint was the difference in Yale global tic severity scale(YGTSS)-total tic severity(TTS) score from baseline after 6 weeks of treatment. The results showed that after 6 weeks of treatment, the declines in YGTSS-TSS score showed no statistically significant difference between the two groups. The difference in YGTSS-TSS score(treatment group-control group) and the 95%CI of the full analysis set(FAS) were-0.17[-1.42, 1.08] and those of per-protocol set(PPS) were 0.29[-0.97, 1.56], which were within the equivalence boundary [-3, 3]. The equivalence test was therefore concluded. The two groups showed no significant differences in the secondary efficacy endpoints of effective rate for TD, total score and factor scores of YGTSS, clinical global impressions-severity(CGI-S) score, traditional Chinese medicine(TCM) response rate, or symptom disappearance rate, and thus a complete evidence chain with the primary outcome was formed. A total of 6 adverse reactions were reported, including 4(2.82%) cases in the treatment group and 2(1.41%) cases in the control group, which showed no statistically significant difference between the two groups. No serious suspected unexpected adverse reactions were reported, and no laboratory test results indicated serious clinically significant abnormalities. The results support the replacement of Os Draconis by Ostreae Concha in the original formula, and the efficacy and safety of the modified formula are consistent with those of the original formula.
Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Male ; Double-Blind Method ; Drugs, Chinese Herbal/therapeutic use* ; Tic Disorders/drug therapy* ; Treatment Outcome

BACKGROUND: The association of systemic inflammatory response index (SIRI) with prognosis of coronary artery disease (CAD) patients has never been investigated in a large sample with long-term follow-up. This study aimed to explore the association of SIRI with all-cause and cause-specific mortality in a nationally representative sample of CAD patients from United States. METHODS: A total of 3386 participants with CAD from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 were included in this study. Cox proportional hazards model, restricted cubic spline (RCS), and receiver operating characteristic curve (ROC) were performed to investigate the association of SIRI with all-cause and cause-specific mortality. Piece-wise linear regression and sensitivity analyses were also performed. RESULTS: During a median follow-up of 7.7 years, 1454 all-cause mortality occurred. After adjusting for confounding factors, higher lnSIRI was significantly associated with higher risk of all-cause (HR = 1.16, 95% CI: 1.09-1.23) and CVD mortality (HR = 1.17, 95% CI: 1.05-1.30) but not cancer mortality (HR = 1.17, 95% CI: 0.99-1.38). The associations of SIRI with all-cause and CVD mortality were detected as J-shaped with threshold values of 1.05935 and 1.122946 for SIRI, respectively. ROC curves showed that lnSIRI had robust predictive effect both in short and long terms. CONCLUSIONS SIRI was independently associated with all-cause and CVD mortality, and the dose-response relationship was J-shaped. SIRI might serve as a valid predictor for all-cause and CVD mortality both in the short and long terms.

Objective:To investigate the protective effect of lovastatin on liver injury in the rats induced by hyperlipidemia,and to elucidate its possible mechanism.Methods:Fifteen SD rats were randomly divided into control group,hyperlipidemia model group,and lovastatin group,with 5 rats in each group.The rats in control group were fed with standard diet,while the rats in hyperlipidemia model group and lovastatin group were fed high-fat diet for 12 weeks.Starting from the 8th week,the rats were administered treatments via gavage once a day for 4 weeks:the rats in lovastatin group received 2 mng·kg-1 lovastatin,while the rats in control group and hyperlipidemia model group received an equal volume of normal saline.The body weights of the rats in various groups were measured at weeks 1,8,9,10,11,and 12 after the experiment began;the histopathology of liver tissue of the rats in various groups was observed using HE staining;the serum levels of total cholesterol(TC),triglycerides(TG),high-density lipoprotein cholesterol(HDL-C),low-density lipoprotein cholesterol(LDL-C),malondialdehyde(MDA),as well as the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),aspartate aminotransferase(AST),and alanine aminotransferase(ALT),and the levels of interleukin-2(IL-2),interleukin-6(IL-6),interleukin-12(IL-12),and tumor necrosis factor-a(TNF-α)of the rats in various groups were detected using commercial kits;the composition of the gut microbiota of the rats in various groups was analyzed by 16S rRNA sequencing.Results:Compared with control group,the body weight of the rats in hyperlipidemia model group was significantly increased from the 8th week of high-fat diet feeding(P＜0.05 or P＜0.01 or P＜0.001).Compared with hyperlipidemia model group,the body weight of the rats in lovastatin group was significantly decreased at weeks 11 and 12(P＜0.05).Compared with control group,the livers of the rats in hyperlipidemia model group appeared rough,pale,enlarged,with blunt edges,and had a granular and greasy texture.Compared with hyperlipidemia model group,the livers of the rats in lovastatin group were light brownish-red,soft,with slightly blunt edges,reduced volume,and less granularity and greasiness.Compared with control group,the liver cells of the rats in hyperlipidemia model group were swollen and disorganized,with pyknotic nuclei,extensive inflammatory cell infiltration,and numerous vacuolar degenerations.Compared with hyperlipidemia model group,the rats in lovastatin group showed significantly reduced hepatocyte swelling and degeneration,more orderly and intact liver cell arrangement,decreased inflammatory cell infiltration,and reduced vacuolar degeneration.Compared with control group,the serum levels of TC,TG,and LDL-C of the rats in hyperlipidemia model group were significantly increased(P＜0.05),and the serum HDL-C level was decreased(P＜0.05).Compared with hyperlipidemia model group,the serum levels of TC,TG,and LDL-C of the rats in lovastation group were significantly decreased(P＜0.05),and the serum HDL-C level was increased(P＜0.05).Compared with control group,the serum MDA levels and the ALT and AST activities of the rats in hyperlipidemia model group were significantly increased(P＜0.05),and the SOD and GSH-Px activities were significantly decreased(P＜0.05).Compared with hyperlipidemia model group,the serum MDA levels and ALT and AST activities of the rats in lovastatin group were decreased(P＜0.05),and the SOD and GSH-Px activities were increased(P＜0.05).Compared with control group,the serum levels of IL-2,IL-6,IL-12,and TNF-α of the rats in hyperlipidemia model group were significantly increased(P＜0.05).Compared with hyperlipidemia model group,the serum levels of IL-2,IL-6,IL-12,and TNF-α of the rats in lovastatin group were significantly decreased(P＜0.05).Compared with control group,the ACE and Chao1 indexes of the rats in hyperlipidemia model group were significantly decreased(P＜0.05).Compared with hyperlipidemia model group,the ACE and Chao1 indexes of the rats in lovastatin group were significantly increased(P＜0.05 or P＜0.01).Compared with control group,the relative abundances of Firmicutes and Proteobacteria of the rats in hyperlipidemia model group were significantly increased(P＜0.001),and the relative abundances of Bacteroidetes and Actinobacteria were decreased(P＜0.001).Compared with hyperlipidemia model group,the relative abundances of Firmicutes and Proteobacteria of the rats in lovastatin group were significantly decreased(P＜0.05 or P＜0.01),while the relative abundances of Bacteroidetes and Actinobacteria showed no significant changes.Compared with control group,the relative abundance of Lactobacillus of the rats in hyperlipidemia model group was significantly decreased(P＜0.001),and the relative abundances of Bacteroides,Desulfovibrio,and Clostridium were significantly increased(P＜0.01 or P＜0.001).Compared with hyperlipidemia model group,the relative abundance of Lactobacillus of the rats in lovastatin group showed no significant change but the relative abundances of Bacteroides,Desulfovibrio,and Clostridium were significantly decreased(P＜0.05 or P＜0.01 or P＜0.001).Conclusion:Lovastatin ameliorates liver injury induced by hyperlipidemia,and the mechanism may be related to its ability to improve gut microbiota composition and inhibit oxidative stress and inflammatory damage.

Objective:To investigate the clinicopathological features and differential diagnosis of male genital system lympho-ma(MGSL).Methods:We retrospectively analyzed the clinicopathological and immunophenotypic features and prognosis of 80 ca-ses of MGSL.Results:The onset age of the MGSL patients ranged from 4 to 85(median 62)years old.All the cases showed non-specificity of the imaging features and clinical manifestations.MGSL was located mainly in the testis(n=66),followed by the pros-tate(n=7),epididymis(n=3),scrotum(n=3)and penile glans(n=1).Diffused large B cell lymphoma(DLBCL)was the most common pathological type(n=62),next came extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue(MALT)(n=7)and other rare types(n=12).During the 1-112-month follow-up of 10 of the 19 patients,1 died at 1 month af-ter diagnosed with prostatic B-lymphoblastic lymphoma(B-LBL)and another 1 died at 50 months after diagnosed with testicular DLBCL.Conclusion:MGSL is rare clinically,mainly of the DLBCL type pathologically,lacking specificity in clinical symptoms and imaging manifestation.The definite diagnosis of the malignancy depends on histopathology combined with related molecular exami-nation and immunohistochemical labeling,and R-CHOP chemotherapy is the first choice for its treatment.

The real-time Delphi method represents a refinement of the classical Delphi technique, designed to overcome limitations such as prolonged study duration and delayed feedback during consensus development. This article, building upon the classical Delphi foundation, systematically elaborates on the application process, advantages, and limitations of the real-time Delphi method. It further presents currently available websites or software capable of facilitating real-time Delphi exercises and offers considerations and recommendations for its application in guideline development, aiming to serve as a reference for relevant researchers.

AIM To investigate effects of petroleum ether fraction from Derris eriocarpa How on glucose and lipid metabolism in a mouse model of metabolic syndrome(MS).METHODS KM mice were fed a high-fat diet and administered streptozotocin intraperitoneally to establish MS models.The MS mice were then randomly assigned to the model group,the metformin hydrochloride group,the lovastatin group,the ursolic acid group,and the high-,medium-and low-dose D.eriocarpa petroleum ether fraction groups,with 10 mice in each group.Ten additional mice maitained on a normal diet served as the normal control group.After 4 weeks of intragastric administration,glucose and lipid metabolism indicators were measured.Hepatic pathological changes were assessed using HE staining and oil red O staining.Liver tissue mRNA expressions of ATF3,PEPCK,FXR,CYP7A1,HNF4ɑ,CYP8B1 and SRB1 were quantified by RT-qPCR.Hepatic protein expressions of ATF3,HNF4ɑ,PEPCK,FXR and CYP7A1 was analyzed by Western blot in MS mice.RESULTS Compared to the model group,the high-dose D.eriocarpa petroleum ether fraction group exhibited significant glucose tolerance improvement(reduced OGTT-AUC,P＜0.01);favorable serum lipid modulation in terms of increased HDL-C levels(P＜0.01)and decreased TG,TC,LDL-C(P＜0.01);reduced renal biomarkers(BUN,SCR)and hepatotoxic indicators of TBA,AST and ALT activities(P＜0.01);alleviated hepatic lipid accumulation and histopathological damage;downregulated mRNA and protein expressions of ATF3,HNF4ɑ and PEPCK,as well as CYP8B1 mRNA expression(P＜0.01);and upregulated mRNA and protein expressions of FXR and CYP7A1,along with SRB1 mRNA expression(P＜0.01).CONCLUSION D.eriocarpa petroleum ether fraction ameliorates glucose and lipid metabolism dysregulation in MS mice by modulating the ATF3/HNF4ɑ/CYP7A1 signaling pathway,consequently eliciting hypoglycemic,hypolipidemic,hepatoprotective and nephroprotective effects.

Objective:To evaluate the clinical efficacy, safety, and adverse effects of selumetinib in the treatment of children with plexiform neurofibromas (PNF).Methods:A retrospective analysis was conducted on the clinical data of 11 children with PNF who were treated with oral selumetinib for at least 9 months at Xuzhou Children′s Hospital from January 2024 to February 2025. The dosage was 25 mg/m2 twice daily. General patient information was collected, and clinical efficacy parameters and adverse events were compared before treatment, at 6 months, and at 9 months post-treatment. Tumor volume changes were assessed using magnetic resonance imaging (MRI) according to the Response Evaluation Criteria in Solid Tumours (RECIST). Pain severity and its impact on daily life were evaluated using the Wong-Baker Faces Pain Rating Scale Revision (FPS-R) and Pain Interference Index (PII). Safety and adverse events were monitored via regular clinical examinations, cardiac ultrasound, and ophthalmologic evaluations, with adverse events graded using Common Terminology Criteria for Adverse Events (CTCAE) v5.0.Results:All 11 patients completed follow-up [9.20-13.60 (10.65±1.64) months]. The cohort included 6 males and 5 females, aged 4.00-14.00 (9.35±3.00) years. At 6 months post-treatment, MRI revealed≥20% tumor volume reduction in 2 patients (2/11), meeting RECIST criteria for partial response (PR). The remaining 9 patients showed no significant tumor changes, though 2 exhibited lightening of café-au-lait macules (CALMs). By 9 months, 5 patients (5/11) achieved PR per RECIST, with residual tumors demonstrating volume reductions below PR thresholds. Nine patients showed further lightening of CALMs. Comparisons of FPS-R scores at 6 (5.27±1.01) and 9 months (3.64±0.81) post-treatment with baseline scores (6.72±1.01) showed statistically significant differences ( F=29.059, P<0.001). FPS-R scores at both 6 months post-treatment ( t=3.365, P=0.007) and 9 months post-treatment ( t=7.889, P<0.001) were significantly lower compared to baseline scores. FPS-R scores at 9 months post-treatment were significantly lower than those at 6 months post-treatment ( t=4.175, P=0.002). The PII at 9 months (15.64±2.86) differed significantly from baseline (19.64±2.66, t=3.396, P=0.003) and 6-month scores (18.27±2.45, t=2.316, P=0.031), whereas no significant difference was observed between 6-month and baseline PII scores ( t=1.256, P=0.225). Five of the 11 children experienced adverse reactions after taking the medicine, mainly manifested as acne, rash, paronychia, and vomiting. The CTCAE grades of all adverse reactions were≤2, and all could be relieved after symptomatic treatment. There were no significant changes in the cardiac ejection fraction and electrocardiogram of the 11 children compared with the baseline. Conclusions:Selumetinib effectively alleviated pain and improved daily function in children with PNF. Prolonged treatment significantly reduced tumor volumes, demonstrating durable efficacy. The drug exhibited a favorable safety profile, with manageable adverse events.

Objective To study the inhibitory effect of secondary metabolites of Pseudomonas aeruginosa(PA)on Candida albicans(CA)and to explore some of the mechanisms.Methods PA and CA strains were i-solated from clinical specimens from the hospital.Then,PA strains with inhibitory effects on CA were screened through cross-line test and co-incubation test,and crude extracts of PA secondary metabolites were prepared,and were tested together with pyocyanin,phenazine-1-carboxylic acid,1-hydroxyphenazine,and 3-ox-ododecyl-l-homoserine lactone(3-oxo-HSL).The inhibitory effects of various PA secondary metabolites on CA were determined through minimum inhibitory concentration test,minimum bactericidal concentration test,time-sterilization curve measurement,and XTT method activity measurement test,and some mechanisms by which PA secondary metabolites inhibited CA were explored.Results The strongest inhibitory effect on CA was 1-hydroxyphenazine,and at a concentration of 6.250 μg/mL,the relative activity of CA decreased to 0.00%.Next were pyocyanin and PA crude extract,and the relative fungal activity of CA decreased to 0.00%at concentrations of 200 and 100 μg/mL.1-hydroxyphenazine,pyocyanin,3-oxo-HSL and PA crude extract all had inhibitory effects on the formation of CA hyphae.Reactive oxygen species(ROS)were generated in CA cells treated with 1-hydroxyphenazine,phenazine 1-carboxylic acid,pyocyanin,and PA crude extract,and the highest levels of ROS were induced by pyocyanin and 1-hydroxyphenazine.Conclusion Phenazine secondary metabolites 1-hydroxyphenazine and pyocyanin have significant inhibitory effects on the growth and activity of CA,and both induce the highest amount of ROS.The quorum-sensing signal molecule 3-oxo-HSL have no in-hibitory effect on CA growth,but have a significant inhibitory effect on the formation of fungal hyphae.