Chen Runfeng, Liu Guanxiong, Sun Xiaochen, Cao Xiankun, He Wenxin, Lin Xixi, Liu Qian, Zhao Jinmin, Pang Yichuan, Li Baoqiang, Qin An
Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Guangxi, 530021, China.
Nanoscale. 2020 Aug 14;12(30):16229-16244. doi: 10.1039/d0nr02848g. Epub 2020 Jul 24.
Osteoclasts are the main cells involved in normal bone remodeling and pathological bone destruction in vivo. Overactivation of osteoclasts can lead to osteolytic diseases, including breast cancer, bone tumors, arthritis, the aseptic loosening of orthopedic implants, and Paget's disease. Excessive reactive oxygen species are the main cause of osteoclast overactivation. We have synthesized chitosan derived nitrogen-doped carbon dots (N-CDs) with a high synthetic yield and the ability to scavenge reactive oxygen species (ROS). N-CDs effectively abrogated RANKL-induced elevation in ROS generation and therefore impaired the activation of NF-κB and MAPK pathways. Osteoclastogenesis and bone resorption was effectively attenuated in vitro. Furthermore, the in vivo administration of N-CDs in mice protected them against lipopolysaccharide (LPS)-induced calvarial bone destruction and breast cancer cell-induced tibial bone loss. Based on the good biocompatibility of N-CDs and the ability to efficiently remove ROS, a nanomaterial treatment scheme was provided for the first time for the clinical treatment of osteolytic diseases.
破骨细胞是体内参与正常骨重塑和病理性骨破坏的主要细胞。破骨细胞的过度活化会导致溶骨性疾病，包括乳腺癌、骨肿瘤、关节炎、骨科植入物的无菌性松动和佩吉特病。过量的活性氧是破骨细胞过度活化的主要原因。我们已经合成了具有高合成产率和清除活性氧（ROS）能力的壳聚糖衍生氮掺杂碳点（N-CDs）。N-CDs有效地消除了RANKL诱导的ROS生成增加，因此损害了NF-κB和MAPK信号通路的激活。在体外有效地减弱了破骨细胞生成和骨吸收。此外，在小鼠体内施用N-CDs可保护它们免受脂多糖（LPS）诱导的颅骨破坏和乳腺癌细胞诱导的胫骨骨质流失。基于N-CDs良好的生物相容性和有效清除ROS的能力，首次为溶骨性疾病的临床治疗提供了一种纳米材料治疗方案。
