Gümbel Denis, Gelbrich Nadine, Napp Matthias, Daeschlein Georg, Kramer Axel, Sckell Axel, Burchardt Martin, Ekkernkamp Axel, Stope Matthias B
Department of Trauma, Reconstructive Surgery and Rehabilitation Medicine, University Medicine Greifswald, Greifswald, Germany
Department of Trauma and Orthopaedic Surgery, BG Klinikum Unfallkrankenhaus Berlin gGmbH, Berlin, Germany.
Anticancer Res. 2017 Mar;37(3):1031-1038. doi: 10.21873/anticanres.11413.
BACKGROUND/AIM: To evaluate the potential involvement of redox-specific signalling pathways in cold atmospheric plasma (CAP)-induced apoptosis on human osteosarcoma cells.
Osteosarcoma cell lines were treated with CAP with or without antioxidative agents and seeded in cell culture plates. Cell proliferation was determined by counting viable cells. Carrier gas-treated cells served as control. Peroxiredoxin (PRX) 1-3 expression and secretion were assessed.
CAP treatment exhibited strongly attenuated proliferation rates. This effect was significantly attenuated by the addition of N-acetylcysteine (NAC). CAP-treated cells exhibited an increase of PRX 1 and 2 10 sec after treatment. The ratio of oxidized to reduced PRX1 and PRX2 was significantly altered with increasing cellular concentration of the oxidized dimer.
Antioxidant supplementation with NAC increases proliferation of CAP-treated osteosarcoma cells, implicating an involvement of redox signalling. Activation of PRX1 and -2 indicate CAP affects redox homeostasis.
背景/目的：评估氧化还原特异性信号通路在冷大气等离子体（CAP）诱导人骨肉瘤细胞凋亡中的潜在作用。
用含或不含抗氧化剂的CAP处理骨肉瘤细胞系，并接种于细胞培养板中。通过计数活细胞来测定细胞增殖。用载气处理的细胞作为对照。评估过氧化物酶（PRX）1 - 3的表达和分泌情况。
CAP处理显著降低了增殖速率。添加N - 乙酰半胱氨酸（NAC）后，这种效应明显减弱。CAP处理的细胞在处理10秒后PRX 1和2的表达增加。随着氧化二聚体细胞浓度的增加，PRX1和PRX2的氧化态与还原态之比发生了显著变化。
补充抗氧化剂NAC可增加CAP处理的骨肉瘤细胞的增殖，这表明氧化还原信号通路参与其中。PRX1和 - 2的激活表明CAP影响氧化还原稳态。
