Spectrum-Effect Relationships Between the Bioactive Ingredient of Syringa oblata Lindl. Leaves and Its Role in Inhibiting the Biofilm Formation of Streptococcus suis

Infectious diseases caused by bacteria and fungi are the major cause of morbidity and mortality across the globe. Multi-drug resistance in these pathogens augments the complexity and severity of the diseases. Various studies have shown the role of biofilms in multi-drug resistance, where the pathogen resides inside a protective coat made of extracellular polymeric substances. Since biofilms directly influence the virulence and pathogenicity of a pathogen, it is optimal to employ a strategy that effectively inhibits the formation of biofilm. Pomegranate is a common food and is also used traditionally to treat various ailments. This study assessed the anti-biofilm activity of a methanolic extract of pomegranate against bacterial and fungal pathogens. Methanolic extract of pomegranate was shown to inhibit the formation of biofilms by Staphylococcus aureus, methicillin resistant S. aureus, Escherichia coli, and Candida albicans. Apart from inhibiting the formation of biofilm, pomegranate extract disrupted pre-formed biofilms and inhibited germ tube formation, a virulence trait, in C. albicans. Characterization of the methanolic extract of pomegranate revealed the presence of ellagic acid (2,3,7,8-tetrahydroxy-chromeno[5,4,3-cde]chromene-5,10-dione) as the major component. Ellagic acid is a bioactive tannin known for its antioxidant, anticancer, and anti-inflammatory properties. Further studies revealed the ability of ellagic acid to inhibit the growth of all species in suspension at higher concentrations (>75 μg ml(-1)) and biofilm formation at lower concentrations (<40 μg ml(-1)) which warrants further investigation of the potential of ellagic acid or peel powders of pomegranate for the treatment of human ailments. Show more

To investigate the effects and the protective mechanism of iridoid glycosides (IG) enriched from Folium syringae leaves on ulcerative colitis (UC) model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats. UC in rats was induced by colonic administration with TNBS. IG (80, 160 and 240 mg/kg) was administered for 2 weeks to experimental colitis rats. The inflammatory degree was assessed by macroscopic score, histology and myeloperoxidase (MPO) activity. Nitric oxide (NO) and malondialdehyde (MDA) levels were measured with biochemical methods. The protein expressions of nuclear factor-kappaBp65 (NF-κBp65) and mRNA expressions of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and NF-κBp65, were determined by immunohistochemistry and real-time quantitative PCR, respectively. IG significantly ameliorated macroscopic damage and histological changes, reduced the activity of MPO, depressed MDA and NO levels and effectively inhibited the protein and mRNA expressions of NF-κBp65, TNF-α and IL-6 in the colon tissues of experimental colitis in a dose-dependent manner. Moreover, the effects of IG (160 mg/kg and 240 mg/kg) were superior to salicylazosulfapyridine (150 mg/kg). We demonstrated for the first time that IG possessed marked protective effects on experimental colitis through its antioxidation and inhibiting inflammatory mediators by down-regulation of the expressions of NF-κBp65. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved. Show more