Impaired homeostasis of copper has been linked to different pathophysiological mechanisms in neurodegenerative diseases and oxidative injury has been proposed as the main mechanism. This study aims to use curcumin, a widely used antioxidative and anti-apoptotic agent, to exert the neuroprotective effect against copper in vitro and illuminate the underlying mechanism. The effect of curcumin was examined by using a cell counting kit-8 assay, flow cytometry, immunofluorescence, spectrophotometer, and western blot. Results revealed that after pretreatment with curcumin for 3 h, copper-induced toxicity and apoptosis show a significant decline. Further experiments showed that curcumin not only decreased the production of ROS and MDA but also increased the activities of the ROS scavenging enzymes SOD and CAT. Moreover, curcumin treatment alleviated the decrease in mitochondrial membrane potential and the nuclear translocation of cytochrome c induced by copper. The protein levels of pro-caspase 3, pro-caspase 9, and PARP1 were up-regulated and the Bax/Bcl-2 ratio was down-regulated in the presence of curcumin. Taken together, our study demonstrates that curcumin has neuroprotective properties against copper in SH-SY5Y cells and the potential mechanisms might be related to oxidative stress and mitochondrial apoptosis.

铜的体内平衡受损与神经退行性疾病的不同病理生理机制有关，氧化损伤被认为是主要机制。本研究旨在使用广泛使用的抗氧化和抗凋亡剂姜黄素在体外发挥对铜的神经保护作用并阐明其潜在机制。姜黄素的作用通过使用细胞计数 kit-8 测定、流式细胞术、免疫荧光、分光光度计和蛋白质印迹来检查。结果表明，姜黄素预处理3 h​​后，铜诱导的毒性和细胞凋亡显着下降。进一步的实验表明，姜黄素不仅降低了 ROS 和 MDA 的产生，而且提高了 ROS 清除酶 SOD 和 CAT 的活性。而且，姜黄素治疗减轻了铜诱导的线粒体膜电位下降和细胞色素 c 的核转位。在姜黄素存在下，前 caspase 3、前 caspase 9 和 PARP1 的蛋白质水平上调，Bax/Bcl-2 比率下调。总之，我们的研究表明姜黄素对 SH-SY5Y 细胞中的铜具有神经保护作用，其潜在机制可能与氧化应激和线粒体凋亡有关。