Our findings, for the first time, demonstrate that luteolin protects against MI/R injury through promoting signalling through the endogenous antioxidant enzyme, peroxiredoxin II, indicating the important beneficial role of this antioxidant system in the heart.

Recently, there is increased incidence of drug-resistant Helicobacter pylori infection. Biofilm formation confers multidrug resistance to bacteria. Moreover, it has been found that the formation of biofilm on the surface of gastric mucosa is an important reason for the difficulty of eradication of H. pylori. The mechanisms underlying H. pylori biofilm formation in vivo have not been elucidated. Reactive oxygen species (ROS) released by the host immune cells in response to H. pylori infection cannot effectively clear the pathogen. Moreover, the extracellular matrix of the biofilm protects the bacteria against ROS-mediated toxicity. This study hypothesized that ROS can promote H. pylori biofilm formation and treatment with low concentrations of hydrogen peroxide (H2O2) promoted this process in vitro. The comparative transcriptome analysis of planktonic and biofilm-forming cells revealed that the expression of SpoT, a (p)ppGpp (guanosine 3'-diphosphate 5'-triphosphate and guanosine 3',5'-bispyrophosphate) synthetase/hydrolase, is upregulated in H2O2-induced biofilms and that knockout of spoT inhibited H. pylori biofilm formation. Additionally, this study examined the key target molecules involved in SpoT regulation using weighted gene co-expression network analysis. The analysis revealed that neutrophil-activating protein (NapA; HP0243) promoted H2O2-induced biofilm formation and conferred multidrug resistance. Furthermore, vitamin C exhibited anti-H. pylori biofilm activity and downregulated the expression of napA in vitro. These findings provide novel insight into the clearance of H. pylori biofilms.

Background Helicobacter pylori has become increasingly resistant to all commonly used clinical antibiotics. Therefore, new anti–H. pylori drugs need to be identified. Recently, quinones were found to inhibit growth of H. pylori with quinone-derived small-molecule compounds identified as having antitumor effects. Methods The minimum inhibitory concentrations of the compounds against H. pylori were measured by agar plate dilution method. The inhibition of biofilm formation by the compounds was assessed by SYTO9-PI double staining. The reactive oxygen species induced by the compounds were detected by DCFH-DA stain. The clearance effects of the compounds for H. pylori in mouse were evaluated by counting colony-forming units and hematoxylin and eosin staining. Results Our results revealed strong inhibition of M5N32 in vitro against H. pylori in both the planktonic and biofilm-forming states. Resistance to M5N32 was not developed in successive generations of the bacteria. In vivo, the combination of M5N32 and omeprazole showed enhanced effects in comparison to the standard triple therapy. M5N32 was nontoxic to normal tissues. Conclusions M5N32 is effective in the treatment of H. pylori infections, providing potential development of anti–H. pylori medicines in the treatment of H. pylori infections.