Furazolidone Increases Survival of Mice Exposed to Lethal Total Body Irradiation through the Antiapoptosis and Antiautophagy Mechanism.

Furazolidone Increases Survival of Mice Exposed to Lethal Total Body Irradiation through the Antiapoptosis and Antiautophagy Mechanism.
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呋喃唑酮通过抗凋亡和抗自噬机制提高暴露于致死性全身辐射的小鼠的存活率

DOI:
10.1155/2021/6610726
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发表时间:
2021
影响因子:
--
通讯作者:
Liu X
Liu X
中科院分区:
生物学2区
文献类型:
--
作者:
Ma S;Jin Z;Liu Y;Liu L;Feng H;Li P;Tian Z;Ren M;Liu X

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暴露于全身照射(TBI)导致剂量和组织特异性致死。然而,目前还没有有效的、无毒的辐射防护措施。在本研究中,小鼠用传统的抗菌剂,FZD,TBI前预处理,FZD对辐射损伤的保护作用进行了评价,通过参数,如脾指数和胸腺指数,肠组织的免疫组化染色,骨髓嗜多染红细胞微核率。肠上皮细胞系IEC-6被用来研究潜在的机制。我们的研究结果表明,FZD管理显着提高致死剂量照射小鼠的生存,减少微核的数量,上调白细胞的数量和免疫器官指数,并恢复TBI后小鼠肠道的完整性。TUNEL和western blot显示FZD通过下调辐射诱导的细胞凋亡和自噬来保护肠组织。同时,FZD可通过抑制细胞凋亡和自噬来保护IEC-6细胞免受辐射诱导的细胞死亡。总之,FZD通过抗凋亡和抗自噬机制在体外和体内保护免受辐射诱导的细胞死亡。
Exposure to total body irradiation (TBI) causes dose- and tissue-specific lethality. However, there are few effective and nontoxic radiation countermeasures for the radiation injury. In the current study, mice were pretreated with a traditional antimicrobial agent, FZD, before TBI; the protective effects of FZD on radiation injury were evaluated by using parameters such as the spleen index and thymus index, immunohistochemical staining of intestinal tissue, and frequency of micronuclei in polychromatophilic erythrocytes of bone marrow. The intestinal epithelial cell line IEC-6 was used to investigate the underlying mechanisms. Our results indicated that FZD administration significantly improved the survival of lethal dose-irradiated mice, decreased the number of micronuclei, upregulated the number of leukocytes and immune organ indices, and restored intestinal integrity in mice after TBI. TUNEL and western blot showed that FZD protected intestinal tissue by downregulating radiation-induced apoptosis and autophagy. Meanwhile, FZD protected IEC-6 cells from radiation-induced cell death by inhibiting apoptosis and autophagy. To sum up, FZD protected against radiation-induced cell death both in vitro and in vivo through antiapoptosis and antiautophagy mechanisms.
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