As an important recycling and degradation system, autophagy is considered to be critical in regulating stem cell differentiation. It has been shown that graphene oxide quantum dots (GOQDs) are a robust biological labelling tool for stem cells with little cytotoxicity. In this study, we explored the role of autophagy in regulating the impact of GOQDs on the odontoblastic differentiation of DPSCs during autophagy. Western blotting and immunofluorescence staining were used to evaluate the autophagic activity of DPSCs. Quantitative PCR, alizarin red S staining, and alkaline phosphatase staining were used to examine DPSC odontoblastic differentiation. The impacts of ROS scavengers on autophagy induction and reactive oxygen species (ROS) levels were also measured. Lentiviral vectors carrying Beclin1 siRNA sequences, as well as autophagy inhibitors (3-MA and bafilomycin A1), were used to inhibit autophagy. Initial exposure to GOQDs increased autophagic activity and enhanced DPSC mineralization. Autophagy inhibition suppressed GOQD-induced odontoblastic differentiation. Moreover, GOQD treatment induced autophagy in a ROS-dependent manner. GOQDs promoted differentiation, which could be modulated via ROS-induced autophagy.

中文翻译：

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氧化石墨烯量子点通过牙髓干细胞中的活性氧物种依赖性自噬途径诱导矿化。

作为重要的循环和降解系统，自噬被认为是调节干细胞分化的关键。研究表明，氧化石墨烯量子点 (GOQDs) 是一种强大的干细胞生物标记工具，几乎没有细胞毒性。在这项研究中，我们探讨了自噬在自噬过程中调节 GOQDs 对 DPSCs 成牙本质细胞分化的影响中的作用。Western印迹和免疫荧光染色用于评估DPSCs的自噬活性。定量 PCR、茜素红 S 染色和碱性磷酸酶染色用于检查 DPSC 成牙本质细胞分化。还测量了 ROS 清除剂对自噬诱导和活性氧 (ROS) 水平的影响。携带 Beclin1 siRNA 序列的慢病毒载体，以及自噬抑制剂（3-MA 和巴弗洛霉素 A1）用于抑制自噬。初次接触 GOQD 会增加自噬活性并增强 DPSC 矿化。自噬抑制抑制了 GOQD 诱导的成牙本质细胞分化。此外，GOQD 治疗以 ROS 依赖性方式诱导自噬。GOQDs 促进分化，这可以通过 ROS 诱导的自噬来调节。