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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

文献类型：期刊论文

作者Guo, Jiaming4; Liu, Tingting4; Ma, Long2; Hao, Wei1; Yan, Hongli2; Li, Taosheng3; Yang, Yanyong4; Cai, Jianming4; Gao, Fu4; Xu, Zhao3
刊名OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
出版日期2020-08-31
卷号2020
ISSN号1942-0900
DOI10.1155/2020/8905860
通讯作者Gao, Fu(gaofusmmu@163.com) ; Xu, Zhao(zhao.xu@inest.cas.cn) ; Liu, Hu(gzsassliuhu@163.com)
英文摘要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.
WOS关键词RELATIVE BIOLOGICAL EFFECTIVENESS ; ACUTE-RADIATION-SYNDROME ; INHIBITION ; ACTIVATION ; SIRT3
资助项目National Natural Science Foundation of China[31900890] ; Key Program of National Natural Science Foundation of China[11635014] ; Shanghai Sailing Program[19YF1459000] ; Naval Medical University Medial Protection Project[WL-MS-02]
WOS研究方向Cell Biology
语种英语
出版者HINDAWI LTD
WOS记录号WOS:000572347600006
资助机构National Natural Science Foundation of China ; Key Program of National Natural Science Foundation of China ; Shanghai Sailing Program ; Naval Medical University Medial Protection Project
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/104151]  
专题中国科学院合肥物质科学研究院
通讯作者Gao, Fu; Xu, Zhao; Liu, Hu
作者单位1.Naval Med Univ, Changhai Hosp, Dept Endocrinol, Shanghai 200433, Peoples R China
2.Naval Med Univ, Changhai Hosp, Dept Reprod, Med Ctr, Shanghai 200433, Peoples R China
3.Chinese Acad Sci, Inst Nucl Energy Safety Technol, Hefei 230031, Anhui, Peoples R China
4.Naval Med Univ, Dept Radiat Med, Coll Naval Med, Shanghai 200433, Peoples R China
推荐引用方式
GB/T 7714		 Guo, Jiaming,Liu, Tingting,Ma, Long,et al. Polydatin Attenuates 14.1 MeV Neutron-Induced Injuries via Regulating the Apoptosis and Antioxidative Pathways and Improving the Hematopoiesis of Mice[J]. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY,2020,2020.
APA Guo, Jiaming.,Liu, Tingting.,Ma, Long.,Hao, Wei.,Yan, Hongli.,...&Liu, Hu.(2020).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,2020.
MLA Guo, Jiaming,et al."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 2020(2020).

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来源：合肥物质科学研究院

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