Furazolidone-based triple and quadruple eradication therapy for Helicobacter pylori infection.

AIM: To evaluate the efficacy of furazolidone-based triple and quadruple therapy in eradicating Helicobacter pylori (H. pylori) in a multi-center randomized controlled trial. METHODS: A total of 720 H. pylori positive patients with duodenal ulcer disease were enrolled at 10 different hospitals in Jiangxi province in China. The patients were randomly assigned to four treatment groups as follows: patients in Groups 1 and 3 received rabeprazole (10 mg), amoxicillin (1000 mg) and furazolidone (100 mg) twice daily for 7 and 10 d, respectively; patients in Groups 2 and 4 received rabeprazole (10 mg), bismuth (220 mg), amoxicillin (1000 mg) and furazolidone (100 mg) twice daily for 7 and 10 d, respectively. The primary outcome measure was H. pylori eradication rate 4 wk after treatment by intention-to-treat and per protocol analysis, while the secondary outcome measures were symptom and sign changes at the end of treatment and 4 wk after the end of treatment, as well as the proportion of patients who developed adverse events. RESULTS: The demographic data of the four groups were not significantly different. Overall, 666 patients completed the scheme and were re-assessed with the (13)C-urea breath test. The intention-to-treat analysis of the H. pylori eradication rates in Groups 1, 2, 3 and 4 were 74.44%, 82.78%, 78.89% and 86.11%, respectively. The H. pylori eradication rate in Group 4 was significantly higher than that in Group 1. According to the per protocol analysis, the H. pylori eradication rates in Groups 1, 2, 3 and 4 were 81.21%, 89.22%, 85.54% and 92.26%, respectively. The H. pylori eradication rate in Group 4 was significantly higher than that in Group 1. The number of adverse events was 15 (8.3%), 16 (8.9%), 15 (8.3%) and 17 (9.4%) in Groups 1, 2, 3 and 4, respectively, including dizziness, vomiting, diarrhea, nausea, skin rash, itchy skin, and malaise. The symptoms were relieved without special treatment in all of the patients. CONCLUSION: Both 7- and 10-d quadruple furazolidone-based therapies achieve satisfactory H. pylori eradication rates.

[Double suicide gene therapy with RNAi targeting to STAT3 inhibits the growth of colorectal carcinoma cells in vitro].

OBJECTIVE: The aim of this study was to construct a recombinant plasmid carrying fusion suicide gene CDglyTK and RNA interference eukaryotic expressing vector targeting to STAT3, and to investigate the effect of double suicide gene combined with RNAi targeting to STAT3 on HCT116 and HUVEC cells in vitro. METHODS: The CD and TK were cloned by polymerase chain reaction (PCR), and fusion gene CDglyTK was inserted into plasmid pEGFP after DNA sequence analysis, enzyme digestion and ligation. The recombinant plasmid was analyzed by PCR amplification and electrophoresis and enzyme digestion. DNA sequences containing small hairpin structure targeting to STAT3 were synthesized and inserted into the vector. The CDglyTK gene expressions in HCT116 and HUVEC cells were examined by reverse transcription-polymerase chain reaction (RT-PCR) after transfection of HCT116 and HUVEC cells. The inhibitory effect of RNA interference vector targeting to STAT3 was analyzed by RT-PCR and Western blot. The effects of 5-FC and GCV on HCT116 and HUVEC cells transfected with the recombinant plasmids were detected by MTT staining. RESULTS: The results of restriction enzyme digestion and PCR amplification and electrophoresis showed that the recombinant pEGFP/CDglyTK was constructed correctly. The mRNA expression of gene CDglyTK was detected in HCT116 and HUVEC cells which transfected with the recombinant plasmid. The results of RT-PCR and Western blot showed that the RNA interference expression vector targeting to STAT3 effectively inhibited the expression of STAT3 in HCT116 cells. The results of MTT test showed that the inhibition ratio of group pEGFP/CDglyTK was (63.72 ± 0.64)%, significantly higher than that of control group (P < 0.05). The inhibition rate of group pEGFP/STAT3 siRNA was (47.02 ± 0.39)%, which was lower than that of group pEGFP/CDglyTK (P < 0.05), and higher than that of control group (P < 0.05). The inhibition rate of group pEGFP/CdglyTK + pEGFP/STAT3 siRNA was (85.10 ± 0.17)%, significantly higher than those of groups pEGFP/CDglyTK and group pEGFP/STAT3 siRNA (P < 0.05). Meanwhile, in HUVEC cells, the inhibition rate of group pEGFP/CDglyTK was (70.24 ± 0.33)%, significantly higher than that of the control group (P < 0.05). The inhibition rate of group pEGFP/STAT3 siRNA was (46.32 ± 0.15)%, significantly lower than that of group pEGFP/CdglyTK (P < 0.05), and higher than that of the control group (P < 0.05). The inhibition rate of group pEGFP/CdglyTK+pEGFP/STAT3 siRNA was (87.10 ± 0.24)%, significantly higher than those of groups pEGFP/CDglyTK and pEGFP/STAT3 siRNA(P < 0.05). CONCLUSION: The recombinant plasmids pEGFP-CDglyTK and pEGFP/STAT3 siRNA have inhibitory effect on HCT116 and HUVEC cells. The killing effects of double suicide gene combined with RNAi targeting to STAT3 are much better than those of single gene therapy.