Li G, Chang X, Luo X, Zhao Y, Wang W, Kang X
Department of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou 570311, China.
Hainan Institute for Food Control(Hainan Experimental Animal Center), Haikou 570314, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2021 Jun 20;41(6):953-959. doi: 10.12122/j.issn.1673-4254.2021.06.21.
To investigate the apoptosis- inducing effect of fucoxanthin in human prostate cancer PC-3 cells and the underlying mechanism.
The viability and apoptosis of PC-3 cells treated with fucoxanthin were analyzed using commercial kits, and the mitochondrial membrane potential, mitochondrial morphology and mitochondrial superoxide were detected using fluorescence probe staining. The contents of ATP, HO, malondialdehyde (MDA), superoxide and the total antioxidant capacity of PC-3 cells were determined. The protein expressions of Bcl-2, Bax and cytochrome c were detected with Western blotting, and the activity of caspase-9 and caspase- 3/7 was detected using corresponding kits.
Fucoxanthin significantly inhibited the viability of PC-3 cells in a time- and dose-dependent manner, and dose-dependently induced apoptosis of the cells ( < 0.05). Fucoxanthin-treated PC-3 cells showed significantly decreased mitochondrial membrane potential, mitochondrial fragmentation and increased superoxide level in the mitochondria ( < 0.05), and these effects of fucoxanthin were dose- dependent. Fucoxanthin dose-dependently decreased ATP level and the total antioxidant capacity of PC-3 cells, increased the contents of HO, MDA and superoxide (all < 0.05), enhanced the protein expressions of Bax and cytochrome c in the cytoplasm, and lowered the protein expressions of Bcl-2 and cytochromes in the mitochondria ( < 0.05).
Fucoxanthin induces apoptosis of PC-3 cells by triggering mitochondrial dysfunction to cause oxidative stress and by activating mitochondria-mediated apoptotic signaling pathways, suggesting its potential in prostate cancer treatment.
研究岩藻黄质对人前列腺癌PC-3细胞的凋亡诱导作用及其潜在机制。
使用商用试剂盒分析经岩藻黄质处理的PC-3细胞的活力和凋亡情况，并用荧光探针染色检测线粒体膜电位、线粒体形态和线粒体超氧化物。测定PC-3细胞中ATP、HO、丙二醛（MDA）、超氧化物的含量以及总抗氧化能力。用蛋白质免疫印迹法检测Bcl-2、Bax和细胞色素c的蛋白表达，并用相应试剂盒检测caspase-9和caspase-3/7的活性。
岩藻黄质以时间和剂量依赖性方式显著抑制PC-3细胞的活力，并呈剂量依赖性诱导细胞凋亡（P<0.05）。经岩藻黄质处理的PC-3细胞线粒体膜电位显著降低，线粒体碎片化，线粒体中超氧化物水平升高（P<0.05），且岩藻黄质的这些作用呈剂量依赖性。岩藻黄质呈剂量依赖性降低PC-3细胞的ATP水平和总抗氧化能力，增加HO、MDA和超氧化物的含量（均P<0.05），增强细胞质中Bax和细胞色素c的蛋白表达，降低线粒体中Bcl-2和细胞色素的蛋白表达（P<0.05）。
岩藻黄质通过引发线粒体功能障碍导致氧化应激并激活线粒体介导的凋亡信号通路来诱导PC-3细胞凋亡，提示其在前列腺癌治疗中的潜力。
