黄芩素抑制金黄色葡萄球菌生物被膜的形成

Inhibition of Staphylococcus aureus Biofilm by Baicalein

细菌生物被膜的形成是导致细菌耐药和引起持续性感染的主要原因之一。本文通过检测黄芩素对金黄色葡萄球菌26112菌株(Staphylococcus aureus 26112,SA26112)多糖细胞间黏附素(polysaccharide intercellular adhesion,PIA)的合成和胞外DNA(extracellular DNA,e DNA)释放量的影响,及其对ica A和cid A基因表达量的影响,探讨黄芩素对金黄色葡萄菌生物被膜形成的抑制作用及其机制。结果显示,黄芩素能抑制SA26112生物被膜的形成,其抑杀SA26112的最低抑菌浓度和最低杀菌浓度均为0.04 mg/m L。0.16 mg/m L黄芩素和256μg/m L环丙沙星单独作用时,均不能杀死其成熟生物被膜内的SA26112细菌,而当二者联用时则可杀死成熟生物被膜内的细菌。黄芩素能显著抑制SA26112菌株PIA的合成、e DNA的释放量及ica A和cid A基因的相对表达量。其中,0.04 mg/m L黄芩素作用SA26112菌株24 h,与对照组相比,e DNA的释放量减少97%,ica A和cid A基因的相对表达量分别减少62%和41%。上述结果表明,黄芩素能抑制SA26112菌株生物被膜的形成,其作用机制可通过降低ica A和cid A的基因表达量,进而影响PIA的合成和e DNA的释放,来抑制金黄色葡萄球菌生物被膜的形成。

The formation of bacterial biofilm is one of the main causes of bacterial resistance and persistent infection. This article aim to investigate the inhibitory effects and mechanisms of baicalein on Staphylococcus aureus biofilm formation by detecting the effects of baicalein on the synthesis of polysaccharide intercellular adhesion（ PIA）,release of extracellular DNA（ e DNA） and expression of ica A and cid A genes in 26112 Staphylococcus aureus strains（ SA26112）. The results showed that baicalein could inhibit the formation of biofilm SA26112,and both the minimum inhibitory concentration and minimum bactericidal concentration of SA26112 biofilm were 0. 04 mg/m L. The application of either0. 16 mg/m L of baicalein or 256 μg/m L of ciprofloxacin could not destroy the SA26112 bacteria with mature biofilm when they were used separately,but it was effective when they were used in combination.Baicaleincan significantly inhibited PIA synthesis,e DNA release and the expression of ica A and cid A of SA26112 strain. After treating SA26112 strain with 0. 04 mg/m L of baicalein for 24 hours,the levels of released e DNA and the relative expression of ica A and cid A were reduced by 97%,62% and 41%,respectively,when compared with control group. The above results show that baicalein can inhibit the biofilm formation of SA26112 strain by reducing the expression of ica A and cid A genes thereby affecting the PIA synthesis and the e DNA release.