HT61 and chlorhexidine (CHX) are both putative membrane-active antimicrobials, which non-specifically target the anionic lipids abundant in bacterial membranes. In model systems, the ability of these antimicrobials to partition into lipid monolayers and increase the permeability of lipid bilayers is dependent upon the presence and proportion of anionic lipids such as phosphatidylglycerol. Despite their apparent similarity in membrane affinity, we have found that HT61 and CHX differ in the extent to which they affect membrane integrity. HT61 was found to be capable of severely disrupting the lipid bilayer, resulting in lysis of Staphylococcus aureus membranes and the release of ATP from protoplasts. CHX, by contrast, does not disrupt the lipid bilayer to a sufficiently large degree to result in lysis of the membrane or release of ATP from S. aureus protoplasts. This suggests that although antimicrobials that interact with the membrane often have a common target, the action they have on the membrane may differ widely and may not be the primary mode of action of the antimicrobial.

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比较HT61和洗必泰对天然和模型金黄色葡萄球菌膜的作用

HT61和洗必太（CHX）都是假定的膜活性抗菌剂，它们非特异性地靶向细菌膜中丰富的阴离子脂质。在模型系统中，这些抗菌剂分配到脂质单层并增加脂质双层的渗透性的能力取决于阴离子脂质（例如磷脂酰甘油）的存在和比例。尽管它们在膜亲和力上有明显相似性，但我们发现HT61和CHX在影响膜完整性的程度上有所不同。发现HT61能够严重破坏脂质双层，导致金黄色葡萄球菌膜溶解并从原生质体释放ATP。相比之下，CHX不会将脂质双层破坏到足够大的程度，不会导致膜溶解或ATP从S释放。金黄色葡萄原生质体。这表明尽管与膜相互作用的抗微生物剂通常具有共同的靶标，但它们对膜的作用可能相差很大，并且可能不是抗微生物剂的主要作用方式。