金属抗菌肽SIF4对金黄色葡萄球菌细胞通透性的影响机制

为探明金属抗菌肽SIF4对金黄色葡萄球菌细胞通透性的影响机制，从胞外碱性磷酸酶活性、细胞表面电位、细胞表面疏水性、细胞内膜通透性和胞内生物大分子泄漏等角度考察了SIF4对细胞通透性的影响。研究发现，SIF4可破坏细胞壁结构完整性，随着抗菌肽质量浓度和温育时间的延长，胞外碱性磷酸酶活性也同步增长，2MIC组与TritonX-100组无显著差异（P>0.05）；细胞表面电位与SIF4质量浓度呈负相关关系；细胞表面疏水性与SIF4质量浓度呈良好的量-效正相关关系；细胞内膜通透性与抗菌肽质量浓度和温育时间呈正相关；胞内生物大分子泄漏与抗菌肽质量浓度和温育时间呈正相关，温育1 h时，胞内蛋白质泄漏呈差异性显著（P<0.05），温育3 h后，2MIC与TritonX-100细胞内生物大分子泄漏差异基本不显著（P>0.05）。结果表明，SIF4可增强细胞通透性并使胞内物质泄漏，还能增强细胞表面疏水性和降低细胞表面电位，使细胞聚沉并诱导细胞坏死。

Mechanism of Metal Antimicrobial Peptide SIF4 against Staphylococcus aureus Cell Permeability

The mechanism of metal antimicrobial peptide SIF4 against cell permeability of Staphylococcus aureus (S.aureus) was explored based on extracellular alkaline phosphatase activity (AKP), cell surface potential (CSP), cell surface hydrophobicity (CSH), cell inner membrane permeability (CIMP) and intracellular macromolecular leakage (IML). The results showed that SIF4 could destroy cell wall structural integrity. With the increasing of antibacterial peptide concentration and incubation time, the activity of extracellular AKP also increased simultaneously, and there was insignificant difference between 2MIC group and TritonX-100 group (P>0.05). The SIF4 concentration had a negative correlation with CSP, and a good dose-effect positive correlation with CSH. Moreover, CIMP and IML had a positive correlation with the antibacterial peptide concentration and incubation time. There was a significant difference in IML (P<0.05) after incubation for 1 h, while there was insignificant difference between the 2MIC and TritonX-100 groups(P>0.05) after 3 h incubation. The findings suggested that SIF4 could enhance cell permea- bility, cause IML leakage, enhance CSH and reduce CSP, inducing cell aggregation and apoptosis.