本研究旨在确定七氟烷（Sev）对鼻咽癌（NPC）恶性行为和线粒体膜电位（MMP）的影响。将 NPC 细胞（5-8F 和 CNE2）暴露于不同浓度的 Sev，然后通过 CCK-8 和集落形成测定法测试增殖，通过流式细胞术测试细胞凋亡，并通过 Transwell 测定法测试侵袭和迁移。此外，还通过测量葡萄糖消耗、乳酸产生和三磷酸腺苷 (ATP) 来检查瓦尔堡效应。通过活性氧（ROS）产生、氧化应激相关指标和线粒体膜电位来评估线粒体功能。 Sev 抑制 5-8F 和 CNE2 细胞增殖、侵袭和迁移，并增强细胞凋亡。此外，Sev 通过减少葡萄糖消耗、乳酸产生和 ATP，以及减少己糖激酶 2 和丙酮酸激酶 M2 型蛋白表达来抑制 Warburg 效应。此外，Sev 还能诱导 ROS 产生和丙二醛含量，并降低超氧化物和谷胱甘肽过氧化物酶水平。最后，Sev 通过诱导 cleaved caspase-3、cleaved caspase-9 和细胞色素 c 蛋白表达以及 MMP 减少，对线粒体稳态造成损害。 Sev通过调节MMP抑制NPC细胞的恶性行为。

This study aims to determine the effect of sevoflurane (Sev) on nasopharyngeal carcinoma (NPC) in malignant behavior and mitochondrial membrane potential (MMP). NPC cells (5-8F and CNE2) were exposed to Sev at different concentrations and then tested for proliferation by CCK-8 and colony formation assays, apoptosis by flow cytometry, and invasion and migration by Transwell assays. In addition, the Warburg effect was examined by measurements of glucose consumption, lactic acid production, and adenosine triphosphate (ATP). Mitochondrial function was evaluated by reactive oxygen species (ROS) production, oxidative stress-related indexes, and mitochondrial membrane potential. Sev suppressed 5-8F and CNE2 cell proliferation, invasion, and migration, and enhanced apoptosis. Moreover, Sev dampened the Warburg effect by reducing glucose consumption, lactic acid production, and ATP, as well as decreasing hexokinase 2 and pyruvate kinases type M2 protein expressions. Also, Sev induced ROS production and malondialdehyde content and reduced superoxide and glutathione peroxidase levels. Finally, Sev caused damage to mitochondrial homeostasis through induction of cleaved caspase-3, cleaved caspase-9, and cytochrome c protein expression and reduction of MMP. Sev inhibits the malignant behavior of NPC cells by regulating MMP.