中文摘要：

目的：细胞冻存、移植器官保存过程中,机体细胞会产生细胞寒冷应激过程,导致细胞产生损伤作用,而其作用机制尚不清楚,本研究通过观察4℃冷暴露对HEK293细胞增殖活性及凋亡的影响,分析线粒体分裂蛋白Drp1在此过程中的表达变化,阐明Drp1在细胞寒冷应激中作用及其机制。方法：采用MTT法观察4℃环境暴露对HEK293细胞损伤的影响,流式细胞术检测细胞凋亡;Western blot方法检测蛋白Drp1、Bcl2表达水平变化,提取线粒体观察线粒体中Drp1表达水平。结果：4℃冷暴露抑制HEK293细胞增殖（P〈0.05）,Drp1线粒体表达水平增高,并向线粒体转位;丙酮酸可以逆转4℃冷暴露对细胞增值抑制,抑制Drp1线粒体表达水平增高,并向线粒体转位,增加细胞中Bcl2表达水平。结论：研究发现细胞寒冷应激可以使细胞凋亡,细胞增殖出现显著抑制,而寒冷应激引起细胞Drp1的线粒体转位,丙酮酸干预后可以对细胞起到保护作用,研究发现丙酮酸可以逆转Drp1的线粒体转位过程,增加Bcl2表达水平,可能是其产生保护作用的机制之一。

英文摘要：

Objective： To observe HEK293 cell proliferation after 4 ~C cold exposure and investigate the role of mitochondrial fission protein Drpl in this process. Methods： MTT assay method was used to detect the HEK293 cell damage after cold stress, flow cytometry method assay for cell apoptosis; Western blot was used to detect protein Drpl and Bcl2 expression level changes, observed mitochondrial Drpl expression levels in extracted mitochondria. Results： 4 ~C cold exposure inhibited the proliferation of HEK293 cells and increased the Drpl mitochondrial expression levels, and mitochondrial translocation; pyruvate can reverse the inhibition of cell proliferation, inhibition of Drpl mitochondrial expression levels, and mitochondrial translocation, increased Bcl2 expression level. Conclusion： Cells cold stress can cause Drpl mitochondrial translocation, cell apoptosis, and pyruvate can reverse Drpl mitochondrial transloeation and increase Bcl2 expression level. This process can play a protective effect on cells.