The epidemiological characteristics and infection risk factors for extrapulmonary tuberculosis in patients hospitalized with pulmonary tuberculosis infection in China from 2017 to 2021.

BACKGROUND: Pulmonary tuberculosis (PTB) complicated with extrapulmonary tuberculosis (EPTB) infection can aggravate the disease, but there have been few reports. METHODS: Retrospective analysis was used to collect the clinical data of PTB patients with pathogen positive in a teaching hospital from 2017 to 2021. We describe the incidence, the invasive site of EPTB patients, and analyze the infection risk factors for PTB with EPTB by univariate and multivariate logistic regression models. We also compared the complications, disease burden with chi-square test and rank-sum test. RESULTS: A total of 1806 PTB were included, of which 263 (14.6%) were complicated with EPTB. The common invasive sites for EPTB were neck lymph nodes (16.49%), intestines (16.13%), and meninges (10.75%). Age ≤ 40 (OR = 1.735; 95%CI [1.267-2.376]; P = 0.001), malnutrition (OR = 2.029; 95%CI [1.097-3.753]; P = 0.022), anemia (OR = 1.739; 95%CI[1.127-2.683]; P = 0.012), and osteoporosis (OR = 4.147; 95%CI [1.577-10.905]; P = 0.004) were all independent risk factors for PTB infection with EPTB. The incidence of extrathoracic hydrothorax, intestinal bacterial infection, urinary tract bacterial infection, and abdominal bacterial infection were higher in patients with PTB with EPTB. PTB with EPTB patients also had longer median hospitalization durations (19 vs. 14 days), during which time they incurred higher total costs, laboratory test costs, imaging examination costs, and drug use costs. CONCLUSION: This study found important risk factors for PTB complicated with EPTB, such as age ≤ 40, malnutrition, anemia, and osteoporosis. PTB with EPTB patients have more extrapulmonary complications and higher hospitalization disease burden.

Prevalent Dominant Acinetobacter baumannii ST191/195/208 Strains in Bloodstream Infections Have High Drug Resistance and Mortality.

Background: Different sequence types of Acinetobacter baumannii (AB) have their own epidemiological characteristics, drug resistance, and toxicity. Methods: AB bloodstream infection (BSI) in the First Affiliated Hospital of Medical College of Zhejiang University from January 2012 to December 2017 were classified by multilocus sequence typing. Clinical data of patients were retrospectively analyzed, drug resistance and toxicity were respectively studied by drug sensitivity and complement killing tests. Results: 247 unduplicated AB strains were collected, and ST191/195/208, the main epidemic dominant strain, accounted for 70.9%. Patients with ST191/195/208 on infection had higher white blood cell (10.8 vs 8.9, p = 0.004), neutrophil% (89.5 vs 86.9, p = 0.005), neutrophil count (9.5 vs 7.1, p = 0.021), D-dimer (6.7 vs 3.8, p = 0.000), total bilirubin (27.0 vs 21.5, p = 0.038), pronatriuretic peptide (324 vs 164, p = 0.042), C-reactive protein (82.5 vs 56.3, p = 0.048), clinical pulmonary infection score (CPIS; 7.33 ± 2.30 vs 6.50 ± 2.72, p = 0.045), and acute physiology and chronic health evaluation-II (APACHE-II; 19.620 ± 5.1850 vs 17.648 ± 6.1251, p = 0.011). Patients with ST191/195/208 had more complications, including pulmonary infection (p = 0.041), septic shock (p = 0.009), and multiple organ failure (p = 0.019). Patients with ST191/195/208 had higher 3 day mortality (24.6% vs 13.9%, p = 0.043), 14 day mortality (46.8% vs 26.8%, p = 0.003), and 28 day mortality (55.0% vs 32.4%, p = 0.001). ST191/195/208 strains had higher drug resistance to most antibiotics, and higher survival rate at 90% normal serum concentration (p < 0.001). Conclusion: ST191/195/208 strains predominate in the hospital and prevails in patients with severe infections with increased multidrug antimicrobial resistance and excessive mortality compared to any other AB stains.

Epidemiology and risk factors of infective endocarditis in a tertiary hospital in China from 2007 to 2016.

BACKGROUND: To explore the trends in epidemiology and the risk factors related to the prognosis of infective endocarditis in a tertiary hospital over the past ten years. METHODS: A retrospective cohort study was performed. A total of 407 consecutive patients who were admitted with infective endocarditis were included. The clinical characteristics and the risk factors related to the prognosis of infective endocarditis during this period were analyzed. RESULTS: A total of 407 patients with infective endocarditis were included, the average age was 48 ± 16 years old with an increasing trend and in-hospital mortality rate was 10.6% and one-year mortality rate was 11.3%. Among patients with underlying heart disease, congenital heart disease was the most common (25.8%), followed by rheumatic heart disease (17.0%) which showed a decreased trend during this period (P < 0.001). There were 222(54.5%) patients with positive blood cultures results and Streptococci (24.6%) was the main pathogens with an increasing trend. There were 403 patients (99%) with surgical indications, but only 235 patients (57.7%) received surgical treatment. Hemodialysis (P = 0.041, OR = 4.697, 95% CI 1.068-20.665), pulmonary hypertension (P = 0.001, OR = 5.308, 95% CI 2.034-13.852), Pitt score ≥ 4 (P < 0.001, OR = 28.594, 95% CI 5.561-148.173) and vegetation length>30 mm (P = 0.011, OR = 13.754, 95% CI 1.832-103.250) were independent risk factors for in-hospital mortality. CONCLUSIONS: There were no significant changes in the overall incidence of infective endocarditis, but the clinical features of infective endocarditis had slightly changed during the past ten years. Streptococci infective endocarditis was still the predominant. Patients with hemodialysis, pulmonary hypertension, Pitt score ≥ 4 and vegetation length>30 mm had an worse in-hospital outcome.

Wza gene knockout decreases Acinetobacter baumannii virulence and affects Wzy-dependent capsular polysaccharide synthesis.

To investigate the virulence of capsular polysaccharide export protein (Wza) in carbapenem-resistant Acinetobacter baumannii and its effect on capsule formation.wza gene knockout and complementation strains were constructed, and changes in bacterial virulence were observed using in vitro adhesion, antiserum complement killing, anti-oxidation experiments, and infections in Galleria mellonella and mice. The effect of wza knockout on the genes wzb and wzc and wzi were assessed by RT-PCR.We successfully constructed wza knockout and complementation strains. Compared with wild-type (WT) strains, wza knockout strains displayed lower adhesion to A549 cells (p = 0.044), lower antiserum complement killing ability (p = 0.001), and lower mortality of G. mellonella (p = 0.010) and mice (p = 0.033). Expression levels of wzb, wzc and wzi were decreased in wza knockout strains. The antioxidant capacity of Wza knockout bacteria was only slightly decreased. Complementation of the wza gene returned the adhesion ability, antiserum complement killing ability, and mortality of G. mellonella and mice to WT levels. Expression of wzb, wzc and wzi was also returned to WT levels following wza complementation.The results clearly demonstrate that Wza is toxic. Wza affects the expression of other proteins of the Wzy capsule polysaccharide synthesis pathway, which affects the assembly, export, and extracellular fixation of capsular polysaccharide, resulting in synergistic effects that decrease bacterial virulence.

The clinical features and prognosis of infective endocarditis in the elderly from 2007 to 2016 in a tertiary hospital in China.

BACKGROUND: Infective endocarditis (IE) especially in the elderly is a serious disease, with a worse prognosis. METHODS: A retrospective cohort study was conducted. A total of 405 patients with definite IE were divided into three groups: 205 patients under 50 years old, 141 patients between 50 and 64 years old and 59 patients over 65 years old. RESULTS: For older patients, clinical symptoms such as fever, anemia, and heart murmur were as common as the younger patients. IE in old patients had more frequent nosocomial origin (P = 0.007) and tended to be more frequent with bad oral hygiene (p = 0.008). The most frequent isolated pathogens in the old groups was streptococci and coagulase-negative staphylococci. The old patients had a lower operation rate (40.7% vs 58.9% vs 62.4%, P = 0.012) and higher in-hospital mortality (20.3% vs 10.6% vs 8.8%, P = 0.044) compared with the younger patients. Surgical treatment was a significant predictor of one-year mortality even after adjusting for the confounders (HR = 2.45, 95% CI 1.027-10.598, P = 0.009). The one-year survival rate was higher for older patients with surgical intervention than those without (95.8% vs 68.6%, P = 0.007). CONCLUSIONS: Older patients with IE presented with more comorbidities, bad oral hygiene, more nosocomial origin and a more severe prognosis than younger patients. Streptococci was the most frequent micro-organisms in this group. Surgery were underused in old patients and those with surgical treatment had better prognosis.

In vitro reduction of colistin susceptibility and comparative genomics reveals multiple differences between MCR-positive and MCR-negative colistin-resistant Escherichia coli.

Objectives: Although resistance to colistin is increasingly reported from clinical settings, the genetic mechanisms that lead to colistin resistance in Escherichia coli have not been fully characterized. Here, we assess the evolution of colistin resistance in clinical isolates of mobilized colistin resistance (MCR)-negative and MCR-positive Escherichia coli. Methods: Spontaneously mutated colistin-resistant progeny were evolved using a step-wise reduction of colistin susceptibility. Resistance phenotypes were confirmed by minimum inhibitory concentration (MIC) determination, and the probable resistance mechanisms were investigated using PCR and reverse transcription-quantitative PCR. Mutated genes of the laboratory-evolved mutants were identified by whole-genome sequencing and comparative genomics. Fitness costs and serum resistance of the mutants were also compared to the corresponding wild types. Results: MCR-negative isolates displayed higher increases in MICs than did MCR-positive isolates following colistin exposure. Upregulation of pmrAB and associated genes was evident among MCR-negative isolates but not MCR-positive isolates. Comparative genomic analysis of mutants and their corresponding wild-types (WTs) revealed numerous mutations in genes encoding membrane transporters and two-component systems. Additionally, MCR-negative mutants exhibited higher fitness costs than MCR-positive mutants compared with their corresponding WTs but displayed similar serum resistance. Conclusion: Our findings reveal multiple differences between MCR-positive and MCR-negative E. coli strains following colistin exposure, which provide reference values for clinical medication.

Comparison of Tigecycline or Cefoperazone/Sulbactam therapy for bloodstream infection due to Carbapenem-resistant Acinetobacter baumannii.

Background: We retrospectively analyzed the effect of tigecycline and cefoperazone/sulbactam therapies on the prognosis of patients with carbapenem-resistant Acinetobacter baumannii bloodstream infection (CRAB-BSI). Methods: CRAB-BSI patients receiving tigecycline therapy or cefoperazone/sulbactam therapy between January 2012 and December 2017 was enrolled, and strict exclusion criteria were followed. The 28-day mortality of patients was analyzed. The impact of cefoperazone/sulbactam therapy on prognosis was evaluated using Cox multivariate regression analysis. The 28-day mortality of patients receiving cefoperazone/sulbactam monotherapy and cefoperazone/sulbactam-based combination therapy was also compared. Results: Three hundred forty eight patients with CRAB-BSI were enrolled in the study. Two hundred ten patients were included after applying the exclusion criteria. Of these, 135 patients received tigecycline therapy and 75 patients received cefoperazone/sulbactam therapy. The 28-day mortality of patients in the latter group was, significantly lower than that of the tigecycline group [29.3% vs. 51.9%; P = 0.001]. Cox multivariate regression analysis revealed that cefoperazone/sulbactam therapy exerted a protective effect on the prognosis of patients [hazard ratio 0.566, 95% confidence interval (0.342-0.940); P = 0.028]. Kaplan-Meier survival curve analysis indicated that the 28-day mortality of patients receiving cefoperazone/sulbactam therapy was lower than that of patients receiving cefoperazone/sulbactam monotherapy, but the difference was not significant (22.2% vs. 40%; P = 0.074). However, the mortality of patients receiving cefoperazone/sulbactam with imipenem/cilastatin was significantly lower than that of patients receiving cefoperazone/sulbactam monotherapy (P = 0.048). Conclusions: Patients treated with cefoperazone/sulbactam therapy had a better clinical outcome. The mortality of patients receiving cefoperazone/sulbactam with imipenem/cilastatin seems to be the lowest.

Retrospective comparative analysis of risk factors and outcomes in patients with carbapenem-resistant Acinetobacter baumannii bloodstream infections: cefoperazone-sulbactam associated with resistance and tigecycline increased the mortality.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) is a rapidly emerging, life-threatening nosocomial infection. This study aimed to explore the risk factors, clinical features, antimicrobial therapy, and outcomes of CRAB bloodstream infections (BSIs). METHODS: This is a retrospective, comparative analysis of data from patients with A. baumannii BSI, treated from 2012 to 2015 at a tertiary teaching hospital. Risk factors associated with CRAB BSI and factors associated with the 28-day mortality were evaluated using logistic analyses. RESULTS: Data from 293 patients with confirmed A. baumannii BSI were included; 242 (82.6%) patients had CRAB BSI and 51 (17.4%) patients had non-CRAB BSI. Risk factors significantly associated with CRAB BSI were a previous intensive care unit (ICU) stay (P=0.029), cefoperazone-sulbactam use (P=0.030), and carbapenem use (P=0.004). Among 236 patients with A. baumannii BSI who were evaluable at 28 days after receiving antibacterial therapy, there were 86 deaths. Factors associated with the 28-day mortality were ICU stay after BSI (P=0.040), readmission within 90 days (P=0.029), Acute Physiology and Chronic Health Evaluation II (APACHE II) score at diagnosis >19 (P=0.012), tigecycline therapy (P=0.021), presence of septic shock (P=0.029), and multiple organ failure (P=0.016). Death rates in patients treated with tigecycline were 53.5% vs 24.1% in patients treated with other agents. Among 186 patients with CRAB BSI evaluable at 28 days, 84 patients died. The associated risk factors were an ICU stay after BSI (P=0.036), APACHE II score >19 at diagnosis (P = 0.002), presence of septic shock (P=0.030), and multiple organ failure (P=0.007). CONCLUSION: This study demonstrated that an ICU stay and cefoperazone-sulbactam or carbapenem use were seen to be the risk factors associated with the development of CRAB BSI. Critical illness and tigecycline therapy were significantly associated with higher mortality of patients with A. baumannii BSI.

In vitro antibacterial effect of fosfomycin combination therapy against colistin-resistant Klebsiella pneumoniae.

OBJECTIVES: Colistin is still a "last-resort" antibiotic used to manage human infections due to multidrug-resistant (MDR) Klebsiella pneumoniae. However, colistin-resistant K. pneumoniae (CR-Kp) isolates emerged a decade ago and had a worldwide distribution. The purpose of this study was to evaluate the genetic data of CR-Kp and identify the antibacterial activity of fosfomycin (FM) alone and in combination with amikacin (AMK) or colistin (COL) against CR-Kp in vitro. METHODS: Three clinical CR-Kp isolates from three patients were collected. Whole-genome sequencing and bioinformatics analysis were performed. The Pharmacokinetics Auto Simulation System 400, by simulating human pharmacokinetics in vitro, was employed to simulate FM, AMK, and COL alone and in combination. Different pharmacodynamic parameters were calculated for determining the antimicrobial effect. RESULTS: Whole-genome sequencing revealed that none of the three isolates contain mcr gene and that no insertion was found in pmrAB, phoPQ, or mgrB genes. We found the antibacterial activity of AMK alone was more efficient than FM or COL against CR-Kp. The area between the control growth and antibacterial killing curves of FM (8 g every 8 hours) combined with AMK (15 mg/kg once daily) was higher than 170 LogCFU/mL·h-1. In addition, the area between the control growth and antibacterial killing curves of FM (8 g every 8 hours) combined with COL (75,000 IU/kg every12 hours) was higher than that of monotherapies (>100 LogCFU/mL·h-1 vs <80 LogCFU/mL·h-1). CONCLUSION: FM (8 g every 8 hours) combined with AMK (15 mg/kg once daily) was effective at maximizing bacterial killing against CR-Kp.

A retrospective, comparative analysis of risk factors and outcomes in carbapenem-susceptible and carbapenem-nonsusceptible Klebsiella pneumoniae bloodstream infections: tigecycline significantly increases the mortality.

BACKGROUND: Carbapenem-nonsusceptible Klebsiella pneumoniae (CnSKP) is rapidly emerging as a life-threatening nosocomial infection. The efficacy of tigecycline in the treatment of bloodstream infections (BSIs) remains controversial. METHODS: Data from a total of 428 patients with carbapenem-susceptible Klebsiella pneumoniae (CSKP) and CnSKP BSIs were collected at a single center between January 2013 and December 2015. A three-part analysis was conducted to identify the risk factors associated with CnSKP, explore prognosis, and evaluate treatments. RESULTS: Data from 428 patients with Klebsiella pneumoniae (KP) BSIs were included, 31.5% (n=135) of them with CnSKP. Multivariate analysis showed that prior hospitalization, urinary catheterization, the use of immunosuppressive agents, prior use of antibiotics, pulmonary disease, and high Acute Physiology and Chronic Health Evaluation (APACHE) II scores were independent risk factors for CnSKP-BSIs. The 30-day mortality was higher in patients with CnSKP than in those with CSKP (58.5% vs 15.4%; P<0.001). In patients with KP-BSIs, neutropenia, multiple organ dysfunction, respiratory failure, CnSKP infection, high APACHE II score, and tigecycline therapy were independently associated with higher mortality risk. Among patients whose APACHE II score was <15, higher mortality rates were observed in patients treated with tigecycline than in those treated with other antibiotics (45.3% vs 7.7%; P<0.001). Central venous catheterization, multiple organ dysfunction, and high APACHE II scores were independent risk factors for death from CnSKP. CONCLUSION: A significant increase in the incidence of CnSKP-BSIs was observed during the study period, with a higher mortality rate found in these patients. Exposure to carbapenems and severe illness were independent risk factors for the development of CnSKP-BSIs, and tigecycline therapy resulted in a significant increase in mortality.

Antibacterial effect evaluation of moxalactam against extended-spectrum ß-lactamase-producing Escherichia coli and Klebsiella pneumoniae with in vitro pharmacokinetics/pharmacodynamics simulation.

OBJECTIVES: The aim of this study was to evaluate the bactericidal effects of moxalactam (MOX), cefotaxime (CTX), and cefoperazone/sulbactam (CFZ/SBT) against extended-spectrum ß-lactamase (ESBL) producing Escherichia coli and Klebsiella pneumoniae, using an in vitro pharmacokinetics (PK)/pharmacodynamics model. METHODS: Two clinical ESBL-producing strains (blaCTX-M-15 positive E. coli 3376 and blaCTX-M-14 positive K. pneumoniae 2689) and E. coli American Type Culture Collection (ATCC)25922 were used in the study. The PK Auto Simulation System 400 was used to simulate the human PK procedures after intravenous administration of different doses of MOX, CTX, and CFZ/SBT. Bacterial growth recovery time (RT) and the area between the control growth curve and bactericidal curves (IE) were employed to assess the antibacterial efficacies of all the agents. RESULTS: The minimum inhibitory concentrations of MOX, CTX, and CFZ/SBT against E. coli ATCC25922, 3376, and 2689 strains were 0.5, 0.5, 0.25; 0.06, >256, 256; and 0.5/0.5, 16/16, 32/32 mg/L. All the agents demonstrated outstanding bactericidal effects against E. coli ATCC25922 (RT >24 h and IE >120 log10 CFU/mL·h-1) with simulating PK procedures, especially in the multiple dose administration models. Against ESBL producers, CTX and CFZ/SBT displayed only weak bactericidal effects, and subsequent regrowth was evident. MOX exhibited potent antibacterial activity against all the strains tested. The values of effective parameters of MOX were much higher than those of CTX and CFZ/SBT (the bacterial RTs with the 3 agents were >24, <4, and <13 h, and the IEs were >110, <10, and <60 log10 CFU/mL·h-1, respectively). CONCLUSION: MOX demonstrated excellent bactericidal effect, which is worthy of further exploration to serve as an alternative therapeutic agent against ESBL-producing Enterobacteriaceae.

In vitro Pharmacokinetics/Pharmacodynamics Evaluation of Fosfomycin Combined with Amikacin or Colistin against KPC2-Producing Klebsiella pneumoniae.

Objectives: The emergence of carbapenem-resistant Enterobacteriaceae, especially Klebsiella pneumoniae, has become a major concern in clinic settings. Combination therapy is gaining momentum to counter the secondary resistance and potential suboptimal efficacy of monotherapy. The aim of this study was to evaluate the bactericidal effect of fosfomycin (FM), amikacin (AMK), or colistin (COL) alone and combinations against KPC2-producing K. pneumoniae using dynamic model by simulating human pharmacokinetics in vitro. Methods: The Pharmacokinetics Auto Simulation System 400 system was employed to simulate different dosing regimens of FM, AMK, and COL alone and combination. Bacterial growth recovery time (RT) and the area between the control growth and antibacterial killing curves (IE) were used as unbiased and comprehensive means for determining the antimicrobial effect. Results: We observed that COL alone was much pronounced than FM or AMK against KPC-Kp. IE of FM (8 g every 8 h) plus AMK (15 mg/kg once-daily) and FM (8 g every 8 h) plus COL (75,000 IU/kg every 12 h) were higher (>170 and >200 LogCFU/mL·h-1, respectively) than that of monotherapies against sensitive strains. Of note, the rate of resistance was lower when using the combination of FM (8 g every 8 h) plus COL (75,000 IU/kg every 12 h) than using COL (75,000 IU/kg every 12 h) alone. Conclusions: The combination of FM (8 g every 8 h) plus AMK (15 mg/kg once-daily) and FM (8 g every 8 h) plus COL (75,000 IU/kg every 12 h) were effective at maximizing bacterial killing and suppressing emergence of resistance.

Up-regulation of pVHL along with down-regulation of HIF-1α by NDRG2 expression attenuates proliferation and invasion in renal cancer cells.

The majority of renal cell carcinomas (RCCs) are characterized by loss of function of the tumor suppressor gene von Hippel Lindau (VHL), which acts as ubiquitin ligase for hypoxia-inducible factor-1α (HIF-1α). In the absence of VHL, HIF-1α protein becomes stabilized and contributes to tumorigenesis. Recent data demonstrate the antitumor efficacy of VHL promoter in RCC cells. This study demonstrates that N-Myc downstream-regulated gene 2 (NDRG2) is a potential regulator of VHL. NDRG2 is involved in proliferation and invasion of cancer cell, furthermore it is frequently down-regulated in renal cell carcinoma. Herein we evaluated the effect of NDRG2 overexpression on proliferation and invasion in human renal cancer cells. The human renal cancer cell line 786-O and A498 were infected with Ad-NDRG2 or Ad-LacZ. Overexpression of NDRG2 not only inhibited the growth of the cells, but also suppressed the invasion. Further study showed that the tumor suppressor gene VHL were up-regulated, whereas transcription factor HIF-1a and vascular endothelial growth factor (VEGF) were down-regulated in 786-O cells infected by Ad-NDRG2. Finally, in a nude mouse model, intratumoral injections of Ad-NDRG2 every 3 days for a total of seven times significantly inhibited the growth and angiogenesis of xenografted 786-O tumors. In conclusion, these data indicate that NDRG2 may be involved in proliferation and invasion by impacting the expression of VHL and HIF-1α. NDRG2 may be an attractive therapeutic target for renal cell carcinoma.

Microarray profiling of HepG2 cells ectopically expressing NDRG2.

Previous studies have demonstrated that N-Myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor that is downregulated in many human cancers and when overexpressed, can inhibit tumor growth and metastasis. However, its molecular function, its modulatory targets, and signaling pathways associated with it remain unclear. Here, in an effort to identify the genes modulated by NDRG2 expression, a microarray study was conducted to detect the expression profile of HepG2 cells overexpressing NDRG2 or LacZ. Gene Ontology (GO) biological process analysis revealed that genes related to G protein signaling pathway were upregulated. Five of them were selected and verified by real-time PCR. Gene sets related to M phase of cell cycle were downregulated. This was in agreement with cell cycle analysis. Signaling pathway analysis demonstrated apparent augmented hematopoietic cell lineage pathway and cell adhesion, but reduced glycosylphosphatidylinositol (GPI)-anchor biosynthesis, protein degradation and SNARE interactions. Furthermore, through motif analysis and experimental validation, we found that the p38 phosphorylation can be increased by NDRG2. Our research provides the molecular basis for understanding the role of NDRG2 in tumor cells and raises interesting questions about its mechanisms and potential use in cancer therapy.

[Alkaloid constituents of Corydalis adunca].

OBJECTIVE: To study the alkaloid component of Corydalis adunca Maxim. METHODS: The constituents were isolated by chromatographic methods, their structures were elucidated by spectroscopic evidences. RESULTS: Three compounds were purified and their structures were identified, they were identified as dorydaline (I), dehydrocorydaline (II), dihydrosanguinarine (III). CONCLUSION: Compounds I , II are isolated from this plant for the first time.