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首页> 外文期刊>Archives of Toxicology >Involvement of Hsp70, a stress protein, in the resistance of long-term culture of PC12 cells against sodium nitroprusside (SNP)-induced cell death
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Involvement of Hsp70, a stress protein, in the resistance of long-term culture of PC12 cells against sodium nitroprusside (SNP)-induced cell death

机译：Hsp70，一种应激蛋白，参与PC12细胞长期培养对硝普钠（SNP）诱导的细胞死亡的抵抗

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Sodium nitroprusside (SNP)-treated PC12 cell line is being used in our laboratory as a cell model of nitric oxide (NO)-mediated damage for in vitro evaluation of potential neuroprotective compounds, thus cell response to SNP must be standardized to gain reproducible data. The NO-donor SNP has been shown to induce cell death at high concentrations in undifferentiated PC12 cells. Differences were found in sensitivity to SNP between cells from short- and long-term cultured cells. After 24-h exposure to 100–500 μM SNP, a decrease of cell viability was observed in both short- (17, 21 and 23rd passages) and long-term cultures (46, 49 and 50th passages), with IC50 values of 312.72 and 462.90 μM, respectively. In cells from early passages, SNP-induced cell death was accompanied by significant increases of LDH leakage, nitrite production, malondialdehyde (MDA) levels, catalase (CAT) activity, cleavage of poly(ADP-ribose)polymerase (PARP) and caspase-3 activation in comparison with those from late passages. Furthermore, untreated and SNP-treated cells from long-term cultures displayed an increase of the stress protein Hsp70 levels when compared with those from short-term cultures. Up-regulated levels of Hsp70 may be associated with cell survival. Therefore, cells may acquire a certain resistance to SNP-induced toxicity associated with an increase in cell passage-dependent Hsp70. The protein Hsp70 might modulate the cellular response to the toxic insult by increasing CAT and GSH-Px activities and decreasing caspase-3 activation. Finally, it is crucial for the standardization of this cell model of neurotoxicity, at least in part, the use of PC12 cells in an optimum and reliable range of passages.
机译：在我们的实验室中，硝普钠（SNP）处理的PC12细胞系被用作一氧化氮（NO）介导的损伤的细胞模型，用于体外评估潜在的神经保护性化合物，因此必须对SNP的细胞反应进行标准化才能获得可重复的数据。已经显示NO供体SNP在未分化的PC12细胞中以高浓度诱导细胞死亡。发现短期和长期培养的细胞对SNP的敏感性存在差异。暴露于100–500μMSNP 24小时后，在短期培养（第17、21和23代）和长期培养（第46、49和50代）中均观察到了细胞活力的下降，IC 50值分别为312.72和462.90μM。在早期传代的细胞中，SNP诱导的细胞死亡伴随着LDH泄漏，亚硝酸盐生成，丙二醛（MDA）水平，过氧化氢酶（CAT）活性，聚（ADP-核糖）聚合酶（PARP）和半胱天冬酶-裂解的显着增加。与较晚传代相比，有3次激活。此外，与来自短期培养的细胞相比，来自长期培养的未处理细胞和经SNP处理的细胞显示出应激蛋白Hsp70水平的增加。 Hsp70的上调水平可能与细胞存活有关。因此，细胞可能获得对SNP诱导的毒性的一定抵抗力，这种毒性与细胞传代依赖性Hsp70的增加有关。 Hsp70蛋白可能通过增加CAT和GSH-Px活性并减少caspase-3激活来调节细胞对毒性损伤的反应。最后，对于这种神经毒性细胞模型的标准化至关重要，至少部分是在最佳和可靠的传代范围内使用PC12细胞。

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