RESUMO
Pseudomonas syringaepv Actinidiae (P. syringae) is a common pathogen causing plant diseases. Limoli proved that its strong pathogenicity is closely related to biofilm state. As a natural bacteriostatic agent with broad-spectrum bactericidal properties, juglone can be used as a substitute for synthetic bacteriostatic agents. To explore the antibacterial mechanism, this study was carried out to examine the inhibitory effect of juglone on cell membrane destruction, abnormal oxidative stress, DNA insertion and biofilm prevention of P. syringae. Results showed that juglone at 20 µg/mL can act against planktogenic P. syringae (107 CFU/mL). Specially, the application of juglone significantly damaged the permeability and integrity of the cell membrane of P. syringae. Additionally, juglone caused abnormal intracellular oxidative stress, and also embedded in genomic DNA, which affected the normal function of the DNA of P. syringae. In addition, environmental scanning electron microscope (ESEM) and other methods showed that juglone effectively restricted the production of extracellular polymers, and then affected the formation of the cell membrane. This study provided a possibility for the development and utilization of natural juglone in plants, especially P. syringae.
Assuntos
Biofilmes/efeitos dos fármacos , Naftoquinonas/farmacocinética , Pseudomonas syringae/fisiologia , Biofilmes/crescimento & desenvolvimento , Relação Dose-Resposta a DrogaRESUMO
High-fat (HF) diets cause obesity, gut microbial dysbiosis and associated disorders and inflammatory bowel disease (IBD) due to increased intestinal permeability, which is an important reason for chronic inflammation and oxidative stress. This study was to investigate the effects and mechanism by which walnut green husk polysaccharides (WGHP) prevents obesity, oxidative stress, inflammation, liver and colon damage in HF diet induced rats. We found that WGHP alleviated HF-induced abnormal weight gain, disordered lipid metabolism, inflammation, oxidative stress, colonic tissue injury and up-regulate the expression level of colonic tight junction protein in the rats. Besides, the administration of WGHP promoted browning of iWAT and thermogenesis in BAT of HF-fed rats, and improved gut microbiota dysbiosis by increasing the bacterial diversity and reducing the relative abundance of potential pathogenic bacteria in the colon of the rats. Furthermore, WGHP consumption not only increased the SCFAs content but also improved the relative abundance of Prevotellaceae and Allobaculum in the gut of rats. Our results suggest that the protective effect of WGHP on metabolic inflammation caused by HF may be due to the regulation of gut microbiota and SCFAs.