ABSTRACT Natural killer (NK) cells are innately immune to the body’s immune system and can actively recognize and kill cancer cells. This study explores the potential for enhancing the killing ability of NK cells by co-culturing the NK cells with the target cells under a static magnetic field (SMF). In this study, NK92-MI cell lines were cultured in the presence of a 0.4-T SMF. The effect of the SMF on NK cell viability was evaluated by means of an MTT assay. Culturing tests were performed with inhibitors of the DAG/IP3, STAT3, ERK, JNK and p38 pathways in order to examine the possible signaling cascade responsible for the SMF effect on the NK92-MI cell viability. Finally, the effect of the SMF on the cytotoxicity of the NK92-MI cells was evaluated by co-culturing the NK cells with K562 leukemia cell lines. The results showed that the application of a 0.4-T SMF significantly increased (p < 0.05) the viability of the NK92-MI cells. Furthermore, the inhibitor tests indicated that the SMF affected cell viability by activating multiple MAPK signaling pathways (ERKs, JNKs, and p38-MAPK). Finally, SMF pre-exposure for 48 hr significantly improved the killing activity of the NK92-MI cells (p < 0.05). That is, pre-exposure to SMF increased the viability of the NK92-MI cells and improved their killing ability against K562 tumor cells. In general, the present results suggest that NK cells pre-exposed to 0.4-T SMF show potential as a tool for immune-therapy treatment of cancer.

中文翻译：

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使用静磁场增强自然杀伤细胞的细胞毒性以增加其活力

摘要 自然杀伤 (NK) 细胞对人体免疫系统具有先天免疫能力，可以主动识别和杀死癌细胞。本研究探索了通过在静磁场 (SMF) 下将 NK 细胞与靶细胞共培养来增强 NK 细胞杀伤能力的潜力。在本研究中，NK92-MI 细胞系在 0.4-T SMF 存在下培养。SMF 对 NK 细胞活力的影响通过 MTT 分析进行评估。使用 DAG/IP3、STAT3、ERK、JNK 和 p38 途径的抑制剂进行培养测试，以检查可能导致 SMF 对 NK92-MI 细胞活力的影响的信号级联反应。最后，通过将 NK 细胞与 K562 白血病细胞系共培养来评估 SMF 对 NK92-MI 细胞的细胞毒性的影响。结果表明，0.4-T SMF 的应用显着增加 (p < 0.05) NK92-MI 细胞的活力。此外，抑制剂测试表明 SMF 通过激活多个 MAPK 信号通路（ERK、JNK 和 p38-MAPK）影响细胞活力。最后，SMF 预暴露 48 小时显着提高了 NK92-MI 细胞的杀伤活性（p < 0.05）。也就是说，预先暴露于 SMF 增加了 NK92-MI 细胞的活力并提高了它们对 K562 肿瘤细胞的杀伤能力。总的来说，目前的结果表明，预先暴露于 0.4-T SMF 的 NK 细胞显示出作为癌症免疫疗法治疗工具的潜力。抑制剂测试表明，SMF 通过激活多个 MAPK 信号通路（ERK、JNK 和 p38-MAPK）影响细胞活力。最后，SMF 预暴露 48 小时显着提高了 NK92-MI 细胞的杀伤活性（p < 0.05）。也就是说，预先暴露于 SMF 增加了 NK92-MI 细胞的活力并提高了它们对 K562 肿瘤细胞的杀伤能力。总的来说，目前的结果表明，预先暴露于 0.4-T SMF 的 NK 细胞显示出作为癌症免疫疗法治疗工具的潜力。抑制剂测试表明，SMF 通过激活多个 MAPK 信号通路（ERK、JNK 和 p38-MAPK）影响细胞活力。最后，SMF 预暴露 48 小时显着提高了 NK92-MI 细胞的杀伤活性（p < 0.05）。也就是说，预先暴露于 SMF 增加了 NK92-MI 细胞的活力并提高了它们对 K562 肿瘤细胞的杀伤能力。总的来说，目前的结果表明，预先暴露于 0.4-T SMF 的 NK 细胞显示出作为癌症免疫疗法治疗工具的潜力。