Department of Radiation Oncology, University of California, Irvine, Irvine, California 92697-2695.
Laboratory of Radiation Oncology, Department of Radiation Oncology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Radiat Res. 2020 Dec 1;194(6):625-635. doi: 10.1667/RADE-20-00060.1.
Persistent vasculature abnormalities contribute to an altered CNS microenvironment that further compromises the integrity of the blood-brain barrier and exposes the brain to a host of neurotoxic conditions. Standard radiation therapy at conventional (CONV) dose rate elicits short-term damage to the blood-brain barrier by disrupting supportive cells, vasculature volume and tight junction proteins. While current clinical applications of cranial radiotherapy use dose fractionation to reduce normal tissue damage, these treatments still cause significant complications. While dose escalation enhances treatment of radiation-resistant tumors, methods to subvert normal tissue damage are clearly needed. In this regard, we have recently developed a new modality of irradiation based on the use of ultra-high-dose-rate FLASH that does not induce the classical pathogenic patterns caused by CONV irradiation. In previous work, we optimized the physical parameters required to minimize normal brain toxicity (i.e., FLASH, instantaneous intra-pulse dose rate, 6.9 · 106 Gy/s, at a mean dose rate of 2,500 Gy/s), which we then used in the current study to determine the effect of FLASH on the integrity of the vasculature and the blood-brain barrier. Both early (24 h, one week) and late (one month) timepoints postirradiation were investigated using C57Bl/6J female mice exposed to whole-brain irradiation delivered in single doses of 25 Gy and 10 Gy, respectively, using CONV (0.09 Gy/s) or FLASH (>106 Gy/s). While the majority of changes found one day postirradiation were minimal, FLASH was found to reduce levels of apoptosis in the neurogenic regions of the brain at this time. At one week and one month postirradiation, CONV was found to induce vascular dilation, a well described sign of vascular alteration, while FLASH minimized these effects. These results were positively correlated with and temporally coincident to changes in the immunostaining of the vasodilator eNOS colocalized to the vasculature, suggestive of possible dysregulation in blood flow at these latter times. Overall expression of the tight junction proteins, occludin and claudin-5, which was significantly reduced after CONV irradiation, remained unchanged in the FLASH-irradiated brains at one and four weeks postirradiation. Our data further confirm that, compared to isodoses of CONV irradiation known to elicit detrimental effects, FLASH does not damage the normal vasculature. These data now provide the first evidence that FLASH preserves microvasculature integrity in the brain, which may prove beneficial to cognition while allowing for better tumor control in the clinic.
持续性的血管异常导致中枢神经系统微环境发生改变,进一步损害血脑屏障的完整性,使大脑暴露于多种神经毒性环境中。传统(CONV)剂量率的标准放射治疗通过破坏支持细胞、血管体积和紧密连接蛋白来引起血脑屏障的短期损伤。虽然目前颅放疗的临床应用采用分次照射来减少正常组织损伤,但这些治疗方法仍会引起严重的并发症。虽然剂量递增可以增强对辐射抵抗肿瘤的治疗效果,但显然需要找到方法来减轻正常组织的损伤。在这方面,我们最近开发了一种新的超高速率 FLASH 照射模式,它不会引起 CONV 照射引起的典型发病模式。在之前的工作中,我们优化了所需的物理参数,以最大限度地降低正常大脑毒性(即 FLASH,瞬时脉冲内剂量率为 6.9·106 Gy/s,平均剂量率为 2500 Gy/s),然后在当前研究中使用这些参数来确定 FLASH 对血管完整性和血脑屏障的影响。我们使用 C57Bl/6J 雌性小鼠进行研究,在单次照射 25 Gy 和 10 Gy 时分别使用 CONV(0.09 Gy/s)或 FLASH(>106 Gy/s),在照射后 24 小时、1 周和 1 个月的早期和晚期时间点进行研究。尽管在照射后 1 天发现的大多数变化都很小,但 FLASH 被发现可减少此时大脑神经发生区域的细胞凋亡水平。在照射后 1 周和 1 个月时,CONV 被发现可诱导血管扩张,这是血管改变的一个典型标志,而 FLASH 则可最大程度地减少这些影响。这些结果与血管舒张因子 eNOS 的免疫染色变化呈正相关,并且在时间上与血管的免疫染色变化一致,这表明在这些后期时间点血流可能存在失调。紧密连接蛋白 occludin 和 claudin-5 的总表达在 CONV 照射后显著降低,但在照射后 1 周和 4 周的 FLASH 照射大脑中保持不变。我们的数据进一步证实,与已知会引起有害影响的 CONV 等剂量照射相比,FLASH 不会损害正常的血管系统。这些数据首次提供了 FLASH 可保持大脑微血管完整性的证据,这可能有益于认知功能,同时在临床治疗中实现更好的肿瘤控制。