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本工作在离体细胞水平观察ZnGl_2对链佐霉素(STZ)诱发的胰岛β细胞损伤的保护作用,并分析其可能的作用机制。结果如下:向培养的胰岛细胞中加入生理盐水和STZ(3mmol/L),孵育12h后,活细胞数由实验前的70万个/ml降至43.93±1.16万个/ml;将ZnCl_2(0.25、0.5、1.0mmol/L)和相同剂量的STZ一同加入细胞,可不同程度地缓解STZ对胰岛的破坏作用,在含不同浓度ZnCl_2的培养液中活细胞数分别恢复至47.39±0.88,58.06±2.29,67.72±1.48万个/ml,与STZ破坏组相比,分别具有显著差异,并呈量效关系。在给予ZnCl_2(1.0mmol/L)的同时,向细胞中加入蛋白合成抑制剂亚胺环已酮(100μg/ml),可翻转ZnCl_2的作用,活细胞数由63.17±2.15万个/ml,又重新减至45.77±0.76万个/ml。单独加亚胺环己酮对活细胞数目无明显影响。用~3H-亮氨酸掺入实验观察ZnCl_2对胰岛细胞蛋白合成的影响发现,单独给予ZnCl_2(1.0mmol/L)仅使蛋白合成轻微增加,与盐水对照组无显著差异;在给ZnCl_2的同时加入STZ,则蛋白合成明显增多,保护组与STZ破坏组比较,差异显著。上述结果表明,增加细胞内蛋白合成,以加强细胞自身对外来损伤的修复力,可能是ZnCl_2保护胰岛细胞的机制之一。
In this study, we observed the protective effect of ZnGl 2 against streptozotocin (STZ) -induced islet β cell injury at the level of cells in vitro and analyzed its possible mechanism. The results were as follows: After adding physiological saline and STZ (3mmol / L) to cultured islet cells, the number of viable cells decreased from 700,000 / ml before the experiment to 43.93 ± 11.600 / ml after incubation for 12 hours; ZnCl2 , 0.5, 1.0mmol / L) and the same dose of STZ were added to the cells, which could relieve the destruction of islets by STZ to varying degrees. The number of viable cells in the medium containing different concentrations of ZnCl 2 were restored to 47.39 ± 0.88,58.06 ± 2.29,67.72 ± 14,800 / ml, respectively, compared with STZ damage group, there are significant differences, and the dose-response relationship. Adding ZnCl 2 (1.0 mmol / L), a protein synthesis inhibitor iminocyclone (100 μg / ml), reversed the effect of ZnCl 2, and the number of viable cells was 63.17 ± 21.500 / ml. Reduce to 45.77 ± 0.76 million / ml. Addition of cycloheximide alone did not affect the number of viable cells. The effect of ZnCl 2 on islet cell protein synthesis was observed by ~ 3H-leucine incorporation experiment. The results showed that ZnCl 2 (1.0 mmol / L) alone increased the protein synthesis only slightly, but no significant difference compared with saline control group; while ZnCl 2 The addition of STZ significantly increased the protein synthesis, and the difference between the protective group and the STZ-damaged group was significant. The above results indicate that the mechanism by which ZnCl 2 can protect pancreatic islet cells may be one of the mechanisms by which the intracellular protein synthesis is increased to enhance the repair ability of the cells against external damage.