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1.
World J Microbiol Biotechnol ; 34(5): 64, 2018 Apr 18.
Article in English | MEDLINE | ID: mdl-29671126

ABSTRACT

Staphylococcus aureus (S. aureus) is a common pathogenic bacterium that causes various diseases in both humans and animals. With the increased prevalence of methicillin-resistant S. aureus, the therapeutic effects of commonly used antibiotics are limited against S. aureus infection. Novel treatment strategies and new antibiotics are needed urgently to address this concern. Many studies have shown that virulence factors secreted from S. aureus play vital roles in their pathogenic processes. Alpha-hemolysin (Hla), an important exotoxin in S. aureus, is one such virulence factor that increases sensitivity of multiple host cells to S. aureus resulting in various diseases. Eriodictyol is a flavonoid compound that exists in many fruits and vegetables. In this study, eriodictyol was demonstrated to inhibit the expression of Hla by hemolysis assays, western blotting, and RT-qPCR at the sub-minimal inhibitory concentration. In live/dead and cytotoxicity assays, the results showed that eriodictyol protected A549 cells against Hla-induced injury in a dose-dependent manner. The minimal inhibitory concentration of eriodictyol against S. aureus was 512 µg/mL. Eriodictyol can downregulate S. aureus Hla at both the expressional and transcriptional levels without affecting S. aureus growth. In addition, cell assays had proved that eriodictyol could protect A549 cells against Hla damage. Eriodictyol could therefore have the potential to treat S. aureus infection targeting Hla.


Subject(s)
Anti-Bacterial Agents/pharmacology , Bacterial Toxins/toxicity , Flavanones/pharmacology , Hemolysin Proteins/drug effects , Hemolysin Proteins/toxicity , Lung Injury/prevention & control , Staphylococcus aureus/drug effects , A549 Cells/drug effects , Bacterial Toxins/genetics , Bacterial Toxins/metabolism , Down-Regulation/drug effects , Gene Expression Regulation, Bacterial/drug effects , Hemolysin Proteins/genetics , Hemolysin Proteins/metabolism , Hemolysis , Humans , Lung Injury/microbiology , Methicillin-Resistant Staphylococcus aureus/drug effects , Methicillin-Resistant Staphylococcus aureus/metabolism , Microbial Sensitivity Tests , Pneumonia, Staphylococcal/microbiology , Pneumonia, Staphylococcal/pathology , Pneumonia, Staphylococcal/prevention & control , Staphylococcus aureus/growth & development , Staphylococcus aureus/metabolism , Staphylococcus aureus/pathogenicity , Virulence Factors/metabolism
2.
J Microbiol Biotechnol ; 27(1): 19-25, 2017 Jan 28.
Article in English | MEDLINE | ID: mdl-27666983

ABSTRACT

Staphylococcus aureus (S. aureus) is a common gram-positive bacterium that causes serious infections in humans and animals. With the continuous emergence of methicillin-resistant S. aureus (MRSA) strains, antibiotics have limited efficacy in treating MRSA infections. Accordingly, novel agents that act on new targets are desperately needed to combat these infections. S. aureus alpha-hemolysin plays an indispensable role in its pathogenicity. In this study, we demonstrate that sclareol, a fragrant chemical compound found in clary sage, can prominently decrease alpha-hemolysin secretion in S. aureus strain USA300 at sub-inhibitory concentrations. Hemolysis assays, western-blotting, and RT-PCR were used to detect the production of alpha-hemolysin in the culture supernatant. When USA300 was co-cultured with A549 epithelial cells, sclareol could protect the A549 cells at a final concentration of 8 µg/ml. The protective capability of sclareol against the USA300-mediated injury of A549 cells was further shown by cytotoxicity assays and live/dead analysis. In conclusion, sclareol was shown to inhibit the production of S. aureus alpha-hemolysin. Sclareol has potential for development as a new agent to treat S. aureus infections.

3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-615364

ABSTRACT

To study the anticoagulant effect of Xiang-Qi-Tang (XQT),the mice model of endotoxemia was established to detect the expression of coagulation factors and their regulatory proteins in serum and aorta.The results showed that XQT could decrease the expression of TF and increase the expression of tPA in the aorta of mice with endotoxemia,and also decrease the expression of sEPCR in the serum.We further found that XQT caused the decrease of sEPCR through the regulation of PKC δ and ADAM17 to contribute the anticoagulation in mice.This study may provide a new strategy for treating endotoxin-induced disease and provide evidences for further researching the pharmacological action of XQT.

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