Abstract The photosensitizer talaporfin has been widely used in photodynamic therapy (PDT), but the mechanism of uptake and excretion has not been identified yet. We do research on the metabolism of talaporfin, i.e., endocytotic uptake and lysosomal degradation. Subcellular localization of talaporfin and lysosome were investigated to certify involvement of endocytosis. Talaporfin was introduced into cell lines transfected with lysosomal-associated membrane protein one Green fluorescent protein (LAMP1-GFP). The localization of fluorescence in cells was analyzed by a confocal fluorescence microscope. The fluorescence of talaporfin matched with LAMP1. Six inhibitors were used to inhibit the uptake of talaporfin in order to identify the endocytosis uptake pathway. It is suggested that clathrin and caveolae endocytosis are involved in talaporfin uptake. To investigate lysosomal degradation, talaporfin was taken up for 1 h and then NH4Cl or Chloroquine (CQ) was added to evaluate the decrease in fluorescence intensity of the cells, and it was clearly shown that CQ inhibited talaporfin degradation. These results lead to the conclusion that talaporfin was taken up into tumor cells by endocytosis and degraded by lysosome.

中文翻译：

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阐明光敏剂他拉泊芬的细胞内摄取和降解机制

摘要 光敏剂他拉泊芬已广泛应用于光动力疗法（PDT），但其吸收和排泄机制尚未确定。我们研究他拉泊芬的代谢，即内吞摄取和溶酶体降解。研究了他拉泊芬和溶酶体的亚细胞定位，以证明内吞作用的参与。他拉泊芬被引入用溶酶体相关膜蛋白一种绿色荧光蛋白 (LAMP1-GFP) 转染的细胞系中。通过共聚焦荧光显微镜分析细胞中荧光的定位。他拉泊芬的荧光与 LAMP1 匹配。六种抑制剂用于抑制他拉泊芬的摄取以鉴定内吞摄取途径。提示网格蛋白和小窝内吞作用参与了他拉泊芬的摄取。为了研究溶酶体降解，将他拉泊芬吸收 1 小时，然后加入 NH4Cl 或氯喹 (CQ) 以评估细胞荧光强度的降低，清楚地表明 CQ 抑制了他拉泊芬的降解。这些结果得出的结论是，他拉泊芬通过内吞作用被吸收到肿瘤细胞中并被溶酶体降解。