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Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

机译:氧化石墨烯和还原的氧化石墨烯通过ERK信号通路诱导神经嗜铬细胞瘤来源的PC12细胞凋亡和细胞周期改变

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摘要

Given the novel applications of graphene materials in biomedical and electronics industry, the health hazards of these particles have attracted extensive worldwide attention. Although many studies have been performed on graphene material-induced toxic effects, toxicological data for the effect of graphene materials on the nervous system are lacking. In this study, we focused on the biological effects of graphene oxide (GO) and reduced graphene oxide (rGO) materials on PC12 cells, a type of traditional neural cell line. We found that GO and rGO exerted significant toxic effects on PC12 cells in a dose- and time-dependent manner. Moreover, apoptosis appeared to be a response to toxicity. A potent increase in the number of PC12 cells at G0/G1 phase after GO and rGO exposure was detected by cell cycle analysis. We found that phosphorylation levels of ERK signaling molecules, which are related to cell cycle regulation and apoptosis, were significantly altered after GO and rGO exposure. In conclusion, our results show that GO has more potent toxic effects than rGO and that apoptosis and cell cycle arrest are the main toxicity responses to GO and rGO treatments, which are likely due to ERK pathway regulation.
机译:鉴于石墨烯材料在生物医学和电子工业中的新应用,这些颗粒对健康的危害已引起全世界的广泛关注。尽管已对石墨烯材料引起的毒性作用进行了许多研究,但仍缺乏有关石墨烯材料对神经系统影响的毒理学数据。在这项研究中,我们集中于氧化石墨烯(GO)和还原的氧化石墨烯(rGO)材料对PC12细胞(一种传统的神经细胞系)的生物学作用。我们发现GO和rGO以剂量和时间依赖性的方式对PC12细胞产生了明显的毒性作用。此外,凋亡似乎是对毒性的反应。通过细胞周期分析检测到GO和rGO暴露后,G0 / G1期PC12细胞数量显着增加。我们发现,GO和rGO暴露后,与细胞周期调控和凋亡相关的ERK信号分子的磷酸化水平显着改变。总之,我们的结果表明,GO具有比rGO更强的毒性作用,凋亡和细胞周期停滞是GO和rGO治疗的主要毒性反应,这很可能是由于ERK途径的调控所致。

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