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Rhizoma Coptidis, Cortex Phellodendri, and berberine were reported to inhibit Helicobacter pylori. However, the underlying mechanism remained elusive. Urease plays a vital role in H. pylori colonization and virulence. In this work, aqueous extracts of Rhizoma Coptidis, Cortex Phellodendri of different origins, and purified berberine were investigated against H. pylori urease and jack bean urease to elucidate the inhibitory capacity, kinetics, and mechanism. Results showed that berberine was the major chemical component in Rhizoma Coptidis and Cortex Phellodendri, and the content of berberine in Rhizoma Coptidis was higher than in Cortex Phellodendri. The IC50 values of Rhizoma Coptidis were significantly lower than those Cortex Phellodendri and purified berberine, of which Coptis chinensis was shown to be the most active concentration- and time-dependent urease inhibitor. The Lineweaver-Burk plot analysis indicated that the inhibition pattern of C. chinensis against urease was noncompetitive for both H. pylori urease and jack bean urease. Thiol protectors (L-cysteine, glutathione, and dithiothreithol) significantly protected urease from the loss of enzymatic activity, while fluoride and boric acid showed weaker protection, indicating the active-site sulfhydryl group was possibly responsible for its inhibition. Furthermore, the urease inhibition proved to be reversible since C. chinensis-blocked urease could be reactivated by glutathione. The results suggested that the anti-urease activity of Rhizoma Coptidis was superior to that of Cortex Phellodendri and berberine, which was believed to be more likely to correlate to the content of total alkaloids rather than berberine monomer. The concentration- and time-dependent, reversible, and noncompetitive inhibition against urease by C. chinensis might be attributed to its interaction with the sulfhydryl group of the active site of urease., (Georg Thieme Verlag KG Stuttgart · New York.)

Aim: To investigate the resistance of Helicobacter pylori (H. pylori) to ciprofloxacin (CIP), levofloxacin (LVX) and moxifloxacin (MOX) in the Beijing area and to elucidate the resistance mechanisms., Methods: Seventy-nine H. pylori clinical strains, isolated from patients who had undergone upper gastrointestinal endoscopy in Peking University First Hospital from 2007 to 2009, were tested for their susceptibility to CIP, LVX and MOX using the E-test method. H. pylori strain 26695 was included in the susceptibility testing as a control strain. According to the minimal inhibitory concentration (MIC) values, a strain was classified as resistant to CIP, LVX or MOX when the MIC was > 1 microg/mL. We amplified by polymerase chain reaction (PCR) and sequenced the quinolone resistance-determining regions of the gyrA and gyrB genes from 29 quinolone-resistant and 16 quinolone-susceptible H. pylori strains selected at random., Results: In this study, the resistance rates of H. pylori to CIP, LVX or MOX were 55.7% (44/79), and the primary resistance rates were 26.6% (21/79). Patients with secondary resistance had received LVX in previous eradication treatments, but not MOX or CIP. Forty-five strains, including 29 CIP, LVX or MOX-resistant strains (MIC: 1.5-32 microg/mL) and 16 susceptible strains, were selected randomly from the 79 strains and used in PCR analysis. Among these 45 strains, 27 resistant strains had mutations in the gyrA gene, including 11 strains with mutations corresponding to Asp-91 (MIC: 2-32 microg/mL), one of which also had a mutation corresponding to Val-150, and 16 strains had mutations at Asn-87 (MIC: 4-32 microg/mL), three of which also had mutations corresponding to Arg-140 or Val-150. In addition, Arg-140, Val-150 or Ala-97 mutations were separately detected in three susceptible strains. Analysis of the gyrB gene showed that one strain of low resistance had a mutation corresponding to Ser-457 that coexisted with an Asp-91 mutation. There was a significant difference in the occurrence of mutations in the gyrA gene between CIP, LVX and MOX-resistant and -susceptible strains (P < 0.05), but 2 resistant strains were found to possess no quinolone resistance-determining region mutations., Conclusion: Resistance is primarily mediated through point mutations in gyrA. Whether other mechanisms are responsible for resistance in strains without mutations in the QRDR should be detected.

Background: A new rapid urine test was developed to detect anti-Helicobacter pylori antibody in urine using the principle of immunochromatography. The accuracy of this test in the Chinese population remains to be defined., Aim: To evaluate a new rapid urine test for the diagnosis of H. pylori infection in the Chinese population., Methods: Eligible patients without previous treatment of H. pylori were recruited. In-house rapid urease test and histology were used as the gold standard. The rapid urine test (RAPIRUN H. pylori antibody) was performed and the results were compared with the gold standard., Results: One hundred and twenty-three patients were eligible for analysis and 61 (50%) were H. pylori positive by the gold standard. The rapid urine test showed a sensitivity, specificity, positive predictive value, negative predictive value and accuracy of 96.7%, 95.2%, 95.2%, 96.7% and 95.9%, respectively. Results were obtained within 20 min and no special laboratory support was required., Conclusions: The rapid urine test by immunochromatography is highly accurate for the diagnosis of H. pylori infection in untreated Chinese patients.

In this study serum anti-urease antibodies of Helicobacter pylori was examined in order to investigate the prevalence of H. pylori infection in 394 children between age 1 and 13. The results showed that the average infection rate was 15.7% with a tendency of increase infection rate with age, and by the age of 12 the H. pylori infection rate reached 30%, which was higher than those found in developed countries. We also noticed that there was a comparatively higher serapositivity among 1 and 7 year olds. This may possibly be due to the close contact between family members and school mates. In addition, the serum positive rate of antibody to H. pylori urease in children with recurrent abdominal pain was much higher than those asymptomatic children (P < 0.05).