正常组织和免疫器官的保护是肿瘤放射治疗过程的关键部分。放射引起的免疫器官损伤（RIOD）通过增加氧化应激和炎症反应而引起多种副反应，导致肿瘤放射治疗的治愈率不理想。本研究的目的是开发一种新型高效的抗辐射纳米粒子，并探讨其保护小鼠脾组织免受辐射的机制。制备了三苯基膦阳离子NIT自由基纳米粒子（NPs-TPP-NIT）并用于保护小鼠的脾脏。小鼠接受X射线照射。研究脾组织组织病理学和血液学参数，以评估 NPs-TPP-NIT 对 X 射线辐射的保护作用。蛋白质组学用于识别与炎症因子调节相关的差异表达蛋白质。此外，还进行了体外和体内实验来评估 NPs-TPP-NIT 对放射治疗的影响。 NPs-TPP-NIT 增加了超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性，并降低了丙二醛水平和活性氧的产生。暴露于 6.0 Gy X 射线辐射后的小鼠脾脏。此外，NPs-TPP-NIT 抑制细胞凋亡，阻断裂解的半胱氨酸天冬氨酸特异性蛋白酶/蛋白酶的激活，上调 Bcl-2 的表达，并下调 Bax 的表达。我们证实，NPs-TPP-NIT 可以阻止电离辐射诱导的 IKK/IκB/NF-κB 激活，从而减轻辐射诱导的脾脏炎症损伤。此外，当用于小鼠肿瘤放疗时，NPs-TPP-NIT没有表现出明显的毒性，也没有赋予明显的肿瘤保护作用。NPs-TPP-NIT可以阻止IKK/IκB/NF-κB信号的激活，减少pro的分泌。 -炎症因子，并促进脾脏中抗炎因子的产生，表现出辐射损伤修复能力，且不降低放射治疗的治疗效果。它表明 NPs-TPP-NIT 作为一种潜在的辐射防护药物，可以保护免疫器官免受辐射引起的损伤。© 2024。作者。

Normal tissue and immune organ protection are critical parts of the tumor radiation therapy process. Radiation-induced immune organ damage (RIOD) causes several side reactions by increasing oxidative stress and inflammatory responses, resulting in unsatisfactory curability in tumor radiation therapy. The aim of this study was to develop a novel and efficient anti irradiation nanoparticle and explore its mechanism of protecting splenic tissue from radiation in mice.Nanoparticles of triphenylphosphine cation NIT radicals (NPs-TPP-NIT) were prepared and used to protect the spleens of mice irradiated with X-rays. Splenic tissue histopathology and hematological parameters were investigated to evaluate the protective effect of NPs-TPP-NIT against X-ray radiation. Proteomics was used to identify differentially expressed proteins related to inflammatory factor regulation. In addition, in vitro and in vivo experiments were performed to assess the impact of NPs-TPP-NIT on radiation therapy.NPs-TPP-NIT increased superoxide dismutase, catalase, and glutathione peroxidase activity and decreased malondialdehyde levels and reactive oxygen species generation in the spleens of mice after exposure to 6.0 Gy X-ray radiation. Moreover, NPs-TPP-NIT inhibited cell apoptosis, blocked the activation of cleaved cysteine aspartic acid-specific protease/proteinase, upregulated the expression of Bcl-2, and downregulated that of Bax. We confirmed that NPs-TPP-NIT prevented the IKK/IκB/NF-κB activation induced by ionizing radiation, thereby alleviating radiation-induced splenic inflammatory damage. In addition, when used during radiotherapy for tumors in mice, NPs-TPP-NIT exhibited no significant toxicity and conferred no significant tumor protective effects.NPs-TPP-NIT prevented activation of IKK/IκB/NF-κB signaling, reduced secretion of pro-inflammatory factors, and promoted production of anti-inflammatory factors in the spleen, which exhibited radiation-induced damage repair capability without diminishing the therapeutic effect of radiation therapy. It suggests that NPs-TPP-NIT serve as a potential radioprotective drug to shelter immune organs from radiation-induced damage.© 2024. The Author(s).