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Testing a Novel Heat-Shock Protein Inducer in the Cellular Model of Traumatic Brain Injury Response
Cell and Tissue Biology Pub Date : 2020-03-12 , DOI: 10.1134/s1990519x20010071
V. F. Lazarev , E. A. Dutysheva , M. A. Trestsova , M. A. Mikeladze , I. A. Utepova , O. N. Chupakhin , I. V. Guzhova , B. A. Margulis

Abstract—

Traumatic brain injury (TBI) induces multiple pathological processes affecting various brain cells. the accumulation of toxic factors in interstitial and cerebrospinal fluid may be a consequence of TBI and massive cell death. The accumulation process, causing so-called “secondary damage,” is not transient and often lasts within days and weeks. We believe that Hsp70 protein can play an important role in reducing the severity of posttraumatic pathological complications. Chaperone Hsp70 is known for its cytoprotective activity, and, therefore, an approach involving its increase in in cells exposed to proapoptotic and proinflammatory factors may turn out to be extremely promising. In support of this idea, we studied the effect of the low molecular weight substance KD-29, which is able to induce the synthesis of Hsp70 in the cellular model of the posttraumatic process. We used rat C6 glioma cells to study the cytotoxic effect of rat cerebrospinal fluid obtained after TBI. We found that the drug KD-29 significantly inhibited the apoptosis process and increased the proliferative activity of C6 cells under conditions of modeling posttraumatic processes.


中文翻译:

在创伤性脑损伤反应的细胞模型中测试新型热休克蛋白诱导剂

摘要-

颅脑外伤(TBI)诱发多种影响各种脑细胞的病理过程。间质和脑脊液中毒性因子的积累可能是TBI和大量细胞死亡的结果。造成所谓“二次破坏”的积累过程不是短暂的,通常持续数天和数周。我们认为,Hsp70蛋白在降低创伤后病理并发症的严重性方面可以发挥重要作用。伴侣蛋白Hsp70以其细胞保护活性而闻名,因此,涉及其增加暴露于促凋亡和促炎性因子的细胞数量的方法可能被证明是非常有前途的。为了支持这一想法,我们研究了低分子量物质KD-29的作用,它能够在创伤后过程的细胞模型中诱导Hsp70的合成。我们使用大鼠C6胶质瘤细胞来研究TBI后获得的大鼠脑脊液的细胞毒性作用。我们发现,在模拟创伤后过程的条件下,药物KD-29可显着抑制细胞凋亡过程并增加C6细胞的增殖活性。
更新日期:2020-03-12
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