Recently, we developed highly fluorescent Ti₃C₂ and Nb₂C Mxene quantum dots (QDs) for labeling of in vitro models. However, the mechanism of the toxicity of the prepared QDs was not explored before. In this study, we addressed the possible mechanism associated with cytotoxicity of the QDs to human umbilical vein endothelial cells (HUVECs). Exposure to up to 100 μg/ml Ti₃C₂ but not Nb₂C QDs for 24 h significantly induced cytotoxicity. The exposure also increased intracellular Ti and Nb elements, indicating the internalization of both types of QDs. None of the QDs promoted interleukin 6 (IL‐6) and IL‐8 releases. Rather, Ti₃C₂ QDs significantly reduced IL‐6 and IL‐8 release, indicating that the toxicity of Ti₃C₂ QDs was not due to elevated inflammatory responses. Exposure to Ti₃C₂ but not Nb₂C QDs resulted in increased LC3B‐II/I ratio and beclin‐1 proteins, biomarkers of autophagy, as well as the accumulation of autophagic substance p62. Ti₃C₂ QDs also more effectively promoted pro‐caspase 3 but not pro‐caspase 8 compared with Nb₂C QDs. Furthermore, pre‐treatment with autophagic modulators altered the cytotoxicity of Ti₃C₂ QDs, which further confirmed the role of autophagic dysfunction in Ti₃C₂ QD‐induced toxicity to HUVECs. In conclusion, the results from this study suggested that high levels of Ti₃C₂ QDs could induce cytotoxicity to HUVECs by inducing the dysfunction of autophagy. Nb₂C QDs appeared to be more biocompatible to HUVECs compared with Ti₃C₂ QDs at the same mass concentrations, which suggested a role of composition of Mxene QDs to determine their toxicity to human endothelial cells.

中文翻译：

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Ti3C2 和 Nb2C Mxene 量子点 (QD) 对人脐静脉内皮细胞的毒性比较

最近，我们开发了用于标记体外模型的高荧光 Ti ₃ C ₂和 Nb ₂ C Mxene 量子点 (QD)。然而，之前没有探索过制备的量子点的毒性机制。在这项研究中，我们解决了与量子点对人脐静脉内皮细胞 (HUVEC) 的细胞毒性相关的可能机制。暴露于高达 100 μg/ml Ti ₃ C ₂而不是 Nb ₂ C QD 24 小时可显着诱导细胞毒性。暴露还增加了细胞内的 Ti 和 Nb 元素，表明两种类型的 QD 都被内化了。没有一个量子点促进白介素 6 (IL-6) 和 IL-8 的释放。相反，Ti ₃ C ₂QDs 显着降低了 IL-6 和 IL-8 的释放，表明 Ti ₃ C ₂ QDs的毒性不是由于炎症反应升高。暴露于 Ti ₃ C ₂而不是 Nb ₂ C QD 导致 LC3B-II/I 比率和 beclin-1 蛋白、自噬生物标志物以及自噬物质 p62 的积累增加。与 Nb ₂ C QDs相比，Ti ₃ C ₂ QDs 也更有效地促进了 pro-caspase 3 而不是 pro-caspase 8 。此外，自噬调节剂的预处理改变了 Ti ₃ C ₂ QDs的细胞毒性，这进一步证实了自噬功能障碍在 Ti 中的作用。₃ C ₂ QD 对 HUVEC 的毒性。总之，这项研究的结果表明，高水平的 Ti ₃ C ₂ QD 可以通过诱导自噬功能障碍来诱导对 HUVEC 的细胞毒性。与相同质量浓度的Ti ₃ C ₂ QD相比，Nb ₂ C QD 似乎对 HUVEC 的生物相容性更高，这表明 Mxene QD 的组成在确定它们对人内皮细胞的毒性方面发挥了作用。