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首页> 外文期刊>Journal of applied toxicology >Comparison of toxicity of Ti(3)C(2)and Nb2C Mxene quantum dots (QDs) to human umbilical vein endothelial cells
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Comparison of toxicity of Ti(3)C(2)and Nb2C Mxene quantum dots (QDs) to human umbilical vein endothelial cells

机译：Ti（3）C（2）和Nb2C mxEntum点（QDS）对人脐静脉内皮细胞的毒性比较

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Recently, we developed highly fluorescent Ti(3)C(2)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 mu g/ml Ti(3)C(2)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, Ti(3)C(2)QDs significantly reduced IL-6 and IL-8 release, indicating that the toxicity of Ti(3)C(2)QDs was not due to elevated inflammatory responses. Exposure to Ti(3)C(2)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. Ti(3)C(2)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 Ti(3)C(2)QDs, which further confirmed the role of autophagic dysfunction in Ti(3)C(2)QD-induced toxicity to HUVECs. In conclusion, the results from this study suggested that high levels of Ti(3)C(2)QDs could induce cytotoxicity to HUVECs by inducing the dysfunction of autophagy. Nb2C QDs appeared to be more biocompatible to HUVECs compared with Ti(3)C(2)QDs at the same mass concentrations, which suggested a role of composition of Mxene QDs to determine their toxicity to human endothelial cells.
机译：最近，我们开发了用于体外模型标记的高荧光Ti（3）C（2）和Nb2C Mxene量子点（QD）。然而，所制备的量子点的毒性机制之前没有被探索过。在这项研究中，我们探讨了量子点对人脐静脉内皮细胞（HUVECs）细胞毒性的可能机制。暴露于高达100μg/ml Ti（3）C（2），但不暴露于Nb2C量子点24小时可显著诱导细胞毒性。暴露也增加了细胞内的Ti和Nb元素，表明这两种类型的量子点都被内化。没有一种QDs促进白细胞介素6（IL-6）和IL-8的释放。相反，Ti（3）C（2）量子点显著减少了IL-6和IL-8的释放，这表明Ti（3）C（2）量子点的毒性并不是由于炎症反应增强所致。暴露于Ti（3）C（2）而非Nb2C量子点会导致LC3B-II/I比率和beclin-1蛋白（自噬的生物标志物）增加，以及自噬物质p62的积累。与Nb2C量子点相比，Ti（3）C（2）量子点也能更有效地促进促半胱天冬酶3，但不能促进促半胱天冬酶8。此外，自噬调节剂预处理改变了Ti（3）C（2）量子点的细胞毒性，这进一步证实了自噬功能障碍在Ti（3）C（2）量子点诱导的HUVEC毒性中的作用。总之，本研究的结果表明，高水平的Ti（3）C（2）量子点可以通过诱导自噬功能障碍而诱导对HUVEC的细胞毒性。在相同质量浓度下，与Ti（3）C（2）量子点相比，Nb2C量子点似乎对HUVEC更具生物相容性，这表明Mxene量子点的组成在确定其对人类内皮细胞的毒性方面发挥了作用。

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