文献类型：期刊文献

英文题名：Hypericin Enhances Paclitaxel-Induced B16-F10 Cell Apoptosis by Activating a Cytochrome c Release-Dependent Pathway

作者：Sun, Liyun[1];Li, Zixuan[1];Shang, Huoli[1];Xin, Xiujuan[1]

机构：[1]East China Univ Sci & Technol, Shanghai, Peoples R China

年份：2021

卷号：12

外文期刊名：FRONTIERS IN PHARMACOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000687231200001)】；

基金：This research was supported by the National Natural Science Fund (F100-4-1784), Open Project for the state Key Laboratory of Bioreactor Engineering of East China University of Science and Technology, and China Scholarship Council (File No. 201906745008).

语种：英文

外文关键词：hypericin; paclitaxel; apoptosis; B16-F10 cells; mitochondrial dysfunction; cytochrome c release

摘要：The enhanced inhibitory effect of paclitaxel (PTX) combined with hypericin (HY) on B16-F10 cells may be realized through the ROS-related cytochrome c release pathway. The apoptotic characteristics of the B16-F10 cells, such as DNA fragmentation, chromatin condensation, and apoptotic body formation, were all enhanced in the combined treatment group. Further investigation showed that the combination of paclitaxel and HY could increase the level of mitochondrial damage and the concentration of cytochrome c, causing the expression of caspase-3 and the cleavage of PARP.(1). Compared with paclitaxel or HY alone, the level of reactive oxygen species (ROS) increased significantly, while glutathione reductase (GR) activity and intracellular glutathione (GSH) levels decreased significantly in the combination group.