Division of Pulmonary, Allergy, and Critical Care, Department of Medicine, University of Pennsylvania Perelman School of Medicine, 3450 Hamilton Walk, Stemmler Hall, Office Suite 227, Philadelphia, PA 19104, USA.
Department of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Int J Mol Sci. 2017 Nov 25;18(12):2525. doi: 10.3390/ijms18122525.
Radiation therapy for the treatment of thoracic malignancies has improved significantly by directing of the proton beam in higher doses on the targeted tumor while normal tissues around the tumor receive much lower doses. Nevertheless, exposure of normal tissues to protons is known to pose a substantial risk in long-term survivors, as confirmed by our work in space-relevant exposures of murine lungs to proton radiation. Thus, radioprotective strategies are being sought. We established that LGM2605 is a potent protector from radiation-induced lung toxicity and aimed in the current study to extend the initial findings of space-relevant, proton radiation-associated late lung damage in mice by looking at acute changes in human lung. We used an ex vivo model of organ culture where tissue slices of donor living human lung were kept in culture and exposed to proton radiation. We exposed donor human lung precision-cut lung sections (huPCLS), pretreated with LGM2605, to 4 Gy proton radiation and evaluated them 30 min and 24 h later for gene expression changes relevant to inflammation, oxidative stress, and cell cycle arrest, and determined radiation-induced senescence, inflammation, and oxidative tissue damage. We identified an LGM2605-mediated reduction of proton radiation-induced cellular senescence and associated cell cycle changes, an associated proinflammatory phenotype, and associated oxidative tissue damage. This is a first report on the effects of proton radiation and of the radioprotective properties of LGM2605 on human lung.
质子束在靶向肿瘤上以更高的剂量进行治疗,同时使肿瘤周围的正常组织接受更低的剂量,从而显著提高了治疗胸部恶性肿瘤的放射疗法。然而,正如我们在与太空相关的对老鼠肺部的质子辐射暴露中所证实的那样,正常组织暴露于质子中已知会带来长期生存者的巨大风险。因此,正在寻求放射保护策略。我们已经证实 LGM2605 是一种有效的辐射诱导肺毒性保护剂,在当前的研究中,我们旨在通过观察人类肺部的急性变化,将最初在与太空相关的、与质子辐射相关的老鼠晚期肺部损伤的发现扩展到现实中。我们使用了器官培养的离体模型,其中保存供体活体人类肺部的组织切片并将其暴露于质子辐射下。我们将预处理过 LGM2605 的供体人类肺精确切割肺切片(huPCLS)暴露于 4 Gy 的质子辐射下,并在 30 分钟和 24 小时后评估与炎症、氧化应激和细胞周期停滞相关的基因表达变化,以及确定辐射诱导的衰老、炎症和氧化组织损伤。我们确定了 LGM2605 介导的减少质子辐射诱导的细胞衰老和相关的细胞周期变化、相关的促炎表型以及相关的氧化组织损伤。这是关于质子辐射对人类肺部的影响以及 LGM2605 的放射保护特性的首次报道。