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Polydatin Attenuates 14.1 MeV Neutron-Induced Injuries via Regulating the Apoptosis and Antioxidative Pathways and Improving the Hematopoiesis of Mice.
Oxidative Medicine and Cellular Longevity Pub Date : 2020-08-31 , DOI: 10.1155/2020/8905860
Jiaming Guo 1 , Tingting Liu 1 , Long Ma 2 , Wei Hao 3 , Hongli Yan 2 , Taosheng Li 4 , Yanyong Yang 1 , Jianming Cai 1 , Fu Gao 1 , Zhao Xu 4 , Hu Liu 1
Affiliation  

With more powerful penetrability and ionizing capability, high energetic neutron radiation (HENR) often poses greater threats than photon radiation, especially on such occasions as nuclear bomb exposure, nuclear accidents, aerospace conduction, and neutron-based radiotherapy. Therefore, there emerges an urgent unmet demand in exploring highly efficient radioprotectants against HENR. In the present study, high-throughput 14.1 MeV neutrons were generated by the high-intensity D-T fusion neutron generator (HINEG) and succeeded in establishing the acute radiation syndrome (ARS) mouse model induced by HENR. A series of preclinical studies, including morphopathological assessment, flow cytometry, peripheral complete blood, and bone marrow karyocyte counting, were applied showing much more serious detriments of HENR than the photon radiation. In specific, it was indicated that surviving fraction of polydatin- (PD-) treated mice could appreciably increase to up to 100% when they were exposed to HENR. Moreover, polydatin contributed much in alleviating the HENR-induced mouse body weight loss, spleen and testis indexes decrease, and the microstructure alterations of both the spleen and the bone marrow. Furthermore, we found that the HENR-damaged hematopoiesis was greatly prevented by PD treatment in such aspects as bone marrow hemocytogenesis, splenocytes balancing, or even the peripheral blood cellularity. The additional IHC investigations revealed that PD could exert potent hematopoiesis-promoting effects against HENR via suppressing apoptosis and promoting the antioxidative enzymes such as HO-1.

中文翻译:


虎杖甙通过调节细胞凋亡和抗氧化途径以及改善小鼠造血来减轻 14.1 MeV 中子引起的损伤。



高能中子辐射(HENR)具有更强的穿透力和电离能力,往往比光子辐射造成更大的威胁,特别是在核弹暴露、核事故、航天传导和中子放射治疗等场合。因此,探索高效的 HENR 辐射防护剂亟待满足。本研究利用高强度DT聚变中子发生器(HINEG)产生高通量14.1 MeV中子,成功建立了HENR诱导的急性辐射综合征(ARS)小鼠模型。一系列临床前研究,包括形态病理学评估、流式细胞术、外周全血和骨髓核细胞计数,显示 HENR 的危害比光子辐射更严重。具体而言,研究表明,当虎杖甙 (PD-) 治疗的小鼠暴露于 HENR 时,其存活率可明显增加至 100%。此外,虎杖甙对减轻HENR引起的小鼠体重减轻、脾脏和睾丸指数下降以及脾脏和骨髓微结构的改变也有很大作用。此外,我们发现PD治疗在骨髓血细胞生成、脾细胞平衡甚至外周血细胞结构等方面都极大地阻止了HENR受损的造血功能。其他 IHC 研究表明,PD 可以通过抑制细胞凋亡和促进 HO-1 等抗氧化酶的产生,对 HENR 发挥有效的造血促进作用。
更新日期:2020-08-31
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