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Antibacterial Mechanism of Dihydrotanshinone I
Natural Product Communications ( IF 1.5 ) Pub Date : 2021-02-23 , DOI: 10.1177/1934578x21996158
Lin Zhao 1, 2 , Yingying Zhao 2 , Jinfeng Wei 2, 3 , Zhenhua Liu 2 , Changqin Li 2, 3, 4 , Wenyi Kang 2
Affiliation  

The antimicrobial activity and the underlying action mechanisms of dihydrotanshinone I against Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, extended-spectrum beta-lactamases Staphylococcus aureus were investigated with Kleihauer-Betke (K-B) test. The antibacterial mechanisms of dihydrotanshinone I were investigated by monitoring the changes in electric conductivity, concentration of AKP, protein content, and patterns of protein electrophoretic bands in sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The antibacterial rings showed that antimicrobial activity of dihydrotanshinone I at 18 mM was stronger to Staphylococcus aureus than to methicillin-resistant Staphylococcus aureus and extended-spectrum beta-lactamases Staphylococcus aureus. The minimum inhibitory concentration (MIC) and IC50 values showed that dihydrotanshinone I had the strongest inhibitory activity against S. aureus (MIC = 280 µM, IC50 = 874 ± 0.01 µM, respectively). Dihydrotanshinone I could increase the electric conductivity, concentration of alkaline phosphatase (AKP) and protein content. The patterns of protein bands in SDS-PAGE were changed obviously. Dihydrotanshinone I also significantly inhibited S. aureus, methicillin-resistant S. aureus, and extended-spectrum beta-lactamases S. aureus, indicating that dihydrotanshinone I can damage the structures of cell wall and cell membrane to increase permeability of cell membrane and release of cell components. Dihydrotanshinone I could influence the synthesis of bacterial protein, destroy the protein, or reject the anabolism or expression of the protein, and finally lead to the loss of normal physiological function of bacteria.



中文翻译:

二氢丹参酮I的抗菌机理

通过Kleihauer-Betke(KB)试验研究了二氢丹参酮I对金黄色葡萄球菌,耐甲氧西林金黄色葡萄球菌,广谱β-内酰胺酶金黄色葡萄球菌的抗菌活性及其潜在的作用机理。通过监测十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)中电导率,AKP浓度,蛋白质含量和蛋白质电泳带模式的变化,研究了二氢丹参酮I的抗菌机制。抗菌环显示,二氢丹参酮I在18 mM时对金黄色葡萄球菌的抗菌活性强于对耐甲氧西林的金黄色葡萄球菌和广谱β-内酰胺酶金黄色葡萄球菌。最小抑菌浓度(MIC)和IC 50值表明,二氢丹参酮I对金黄色葡萄球菌的抑菌活性最强(分别为MIC = 280 µM,IC 50 = 874±0.01 µM)。二氢丹参酮I可以增加电导率,碱性磷酸酶(AKP)的浓度和蛋白质含量。SDS-PAGE中蛋白质条带的模式发生了明显变化。二氢丹参酮I还显着抑制金黄色葡萄球菌,耐甲氧西林的金黄色葡萄球菌和广谱β-内酰胺酶金黄色葡萄球菌,表明二氢丹参酮I可以破坏细胞壁和细胞膜的结构,从而增加细胞膜的通透性和细胞成分的释放。二氢丹参酮I可能会影响细菌蛋白质的合成,破坏蛋白质或排斥蛋白质的合成代谢或表达,最终导致细菌正常生理功能的丧失。

更新日期:2021-02-24
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