McCauley R L, Li Y Y, Chopra V, Herndon D N, Robson M C
Skin Tissue Culture Laboratory, Shriners Burns Institute, Galveston, Texas.
J Surg Res. 1994 Apr;56(4):378-84. doi: 10.1006/jsre.1994.1059.
Topical antimicrobial agents, silver sulfadiazine (SSD) and mafenide acetate (MA), have been associated with delayed wound healing. Previous in vitro studies with human dermal fibroblasts (HDF) have shown progressive cellular cytotoxicity with increasing concentrations of SSD and MA. However, preexposure of HDF to epidermal growth factor, basic fibroblast growth factor, or platelet-derived growth factor has resulted in cytoprotection of HDF against 0.01 and 0.03% concentrations of SSD as determined by phase-contrast microscopy (PCM), hemocytometer cell counts, and total cellular protein content. PCM, however, showed slower destruction of HDF at the 0.05% concentration of SSD. These data suggest that cells activated by growth factors either take up less SSD or are more resistant to the direct cytotoxic effects of this drug.
局部抗菌剂，磺胺嘧啶银（SSD）和醋酸甲磺灭脓（MA），与伤口愈合延迟有关。先前用人皮肤成纤维细胞（HDF）进行的体外研究表明，随着SSD和MA浓度的增加，细胞毒性逐渐增强。然而，通过相差显微镜（PCM）、血细胞计数器细胞计数和总细胞蛋白含量测定，将HDF预先暴露于表皮生长因子、碱性成纤维细胞生长因子或血小板衍生生长因子后，HDF对0.01%和0.03%浓度的SSD具有细胞保护作用。然而，PCM显示，在0.05%浓度的SSD下，HDF的破坏速度较慢。这些数据表明，由生长因子激活的细胞要么摄取较少的SSD，要么对这种药物的直接细胞毒性作用更具抗性。
