Tianjin Key Laboratory of Low Dimensional Materials Physics and Preparing Technology, School of Sciences, Tianjin University, Tianjin 300350, China.
Department of Neurosurgery and Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Tianjin Medical University General Hospital, Tianjin 300052, China.
J Mater Chem B. 2020 Mar 18;8(11):2321-2330. doi: 10.1039/c9tb02447f.
Free radical-induced oxidative damage and nitrosative stress have been identified as key factors in neuroinflammation responses after traumatic brain injury (TBI), with which reactive oxygen and nitrogen species (RONS), especially nitrogen signaling molecules, are strongly associated. Here, we prepared ultrasmall carbon dot (CD) by using a simple and facile method. In vitro assessment experiments show that the antioxidative CD exhibits an ultrahigh target-scavenging effect for nitrogen signaling molecules, especially the highly reactive ˙NO and ONOO-. However, CD can only partially eliminate conventional oxygen radials such as O2˙- and ˙OH, indicating CD has a preference for RNS modulation. Moreover, in vitro cell experiments and in vivo mice experiments reveal that CD can reduce the reactive oxygen species (ROS) level and lipid peroxidation, enhance superoxide dismutase (SOD) activity and GSSG level, and further improve the survival rate of neuron cells and TBI mice. These results declare that antioxidative CD could serve as an effective therapeutic for TBI.
自由基诱导的氧化损伤和硝化应激已被确定为创伤性脑损伤 (TBI) 后神经炎症反应的关键因素，其中活性氧和氮物种 (RONS)，特别是氮信号分子，与这些因素密切相关。在这里，我们采用一种简单易行的方法制备了超小的碳点 (CD)。体外评估实验表明，抗氧化 CD 对氮信号分子，特别是高反应性˙NO 和 ONOO-，具有超高的靶向清除作用。然而，CD 只能部分消除传统的含氧自由基，如 O2˙-和˙OH，表明 CD 对 RNS 调节具有偏好性。此外，体外细胞实验和体内小鼠实验表明，CD 可以降低活性氧 (ROS) 水平和脂质过氧化，增强超氧化物歧化酶 (SOD) 活性和 GSSG 水平，进一步提高神经元细胞和 TBI 小鼠的存活率。这些结果表明，抗氧化 CD 可以作为 TBI 的有效治疗方法。
