In this work, the effects of cold atmospheric-pressure plasma (CAP) on glioblastoma are evaluated comprehensively. After CAP treatment, U251 cell viability, migration, and invasion functions were inhibited, while an appropriate dose of CAP had no inhibitory effect on human brain glial cell line cells. Western blots indicated that expression of caspase-3 was upregulated with ki-67 expression downregulated. Moreover, mitochondrial membrane potential decreased, and energy metabolisms of U251 cells were influenced afterward. TUNEL assays and comet assays suggested the DNA damage of U251 cells after CAP treatment. Furthermore, as one of the DNA damage responses associated pathways, the AKT (AKT8 virus oncogene cellular homolog) signaling pathway was also indicated in the work. The findings raise great promise for clinical applications of CAP in glioblastoma treatments.

中文翻译：

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冷常压等离子体在体外和体内通过 DNA 损伤和 AKT 去磷酸化选择性抑制胶质母细胞瘤

在这项工作中，全面评估了冷常压等离子体（CAP）对胶质母细胞瘤的影响。CAP处理后，U251细胞的活力、迁移和侵袭功能均受到抑制，而适当剂量的CAP对人脑胶质细胞系细胞无抑制作用。Western印迹表明caspase-3表达上调，ki-67表达下调。此外，线粒体膜电位下降，U251细胞能量代谢受到影响。TUNEL 测定和彗星测定表明 CAP 处理后 U251 细胞的 DNA 损伤。此外，作为DNA损伤反应相关通路之一，AKT（AKT8病毒癌基因细胞同源物）信号通路也被指出。这些发现为 CAP 在胶质母细胞瘤治疗中的临床应用带来了巨大的希望。