Wang Yu, Pei Zejun, Lou Zaixiang, Wang Hongxin
The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, 214122, People's Republic of China.
School of Food Science and Technology, Jiangnan University, Wuxi, 214122, People's Republic of China.
Infect Drug Resist. 2021 Feb 5;14:435-448. doi: 10.2147/IDR.S285690. eCollection 2021.
The opportunistic pathogen can form biofilms, resulting in drug resistance with great risk to medical treatment.
We investigated the ability of to form biofilms on different materials, as well as the inhibitory and eradicating effects of cordycepin on biofilm. The action mechanism of cordycepin against biofilm was studied by crystal violet staining, XTT [2, 3-bis (2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction method, phenol-sulfuric acid method, cellular superficial hydrophobicity (CSH) assay, and confocal laser scanning microscope observation. We also evaluated the acute toxicity of cordycepin in vivo.
The results showed facile formation of biofilms by on polypropylene. The 50% minimum inhibitory concentration (MIC) of cordycepin was 0.062 mg/mL. A concentration of 0.125 mg/mL significantly decreased biofilm formation, metabolic activity, secretion of extracellular polysaccharides, and relative CSH. Cordycepin could inhibit biofilm formation at low concentration without affecting fungal growth. In addition, cordycepin effectively eradicated 59.14% of mature biofilms of at a concentration of 0.5 mg/mL. For acute toxicity, the LD (50% of lethal dose) of cordycepin was determined as higher than 500 mg/kg for mice.
The results of this study show that cordycepin significantly inhibited and eradicated biofilms by decreasing metabolic activity, the ratio of living cells, the hydrophobicity, and damaging the extracellular polysaccharides of biofilm. These findings should facilitate more effective application of cordycepin and suggest a new direction for the treatment of fungal infections.
机会性病原体可形成生物膜,导致耐药性,给医疗带来巨大风险。
我们研究了[病原体名称未给出]在不同材料上形成生物膜的能力,以及虫草素对生物膜的抑制和根除作用。通过结晶紫染色、XTT [2, 3-双(2-甲氧基-4-硝基-5-磺基苯基)-2H-四唑-5-甲酰苯胺] 还原法、苯酚-硫酸法、细胞表面疏水性(CSH)测定以及共聚焦激光扫描显微镜观察,研究了虫草素对生物膜的作用机制。我们还评估了虫草素在体内的急性毒性。
结果表明,[病原体名称未给出]在聚丙烯上易于形成生物膜。虫草素的50%最小抑菌浓度(MIC)为0.062 mg/mL。浓度为0.125 mg/mL时可显著降低生物膜形成、代谢活性、细胞外多糖分泌以及相对CSH。虫草素在低浓度时可抑制生物膜形成而不影响真菌生长。此外,虫草素在浓度为0.5 mg/mL时可有效根除59.14%的[病原体名称未给出]成熟生物膜。对于急性毒性,虫草素对小鼠的半数致死量(LD)测定结果高于500 mg/kg。
本研究结果表明,虫草素通过降低代谢活性、活细胞比例、疏水性以及破坏生物膜的细胞外多糖,显著抑制和根除生物膜。这些发现应有助于更有效地应用虫草素,并为真菌感染的治疗提供新方向。