Clinical Research Center, The First Affliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou, China.
Department of Anesthesiology, Tongren Municipal People's Hospital, Tongren, Guizhou, China.
Environ Toxicol. 2020 Sep;35(9):922-929. doi: 10.1002/tox.22928. Epub 2020 Apr 15.
Excessive fluoride exposure contributes to neurotoxic effects. Emodin exhibits antioxidative functions in the central nervous system (CNS); however, its neuroprotective mechanism against fluoride remains to be elucidated. Our aim was to explore the neuroprotective efficacy and the possible mechanisms of emodin. In our study, synaptic proteins and oxidative stress damage were examined after human neuroblastoma SH-SY5Y cells were treated with high doses of NaF for 24 hours. Moreover, pretreatment with emodin was used to shed light on the neuroprotective effects in NaF-induced toxicity in SH-SY5Y cells. We found that NaF significantly lowered the protein expressions of SNAP 25, synaptophysin and PSD 95 in SH-SY5Y cells. In addition, NaF exposure increased the protein expression of p-ERK1/2 and decreased the protein expressions of Nrf2 and HO-1, as well as facilitated increasing ROS, 4-hydroxynonenal (4-HNE), and 8-Hydroxy-2'-deoxyguanosine (8-OHdG). Pretreatment with emodin significantly recovered these alterations caused by NaF. These data implied that the neuroprotective effects of emodin and pointed to the promising utilization for protecting against neurotoxicity induced by fluoride.
过量氟暴露会导致神经毒性。大黄素在中枢神经系统（CNS）中具有抗氧化功能；然而，其对氟化物的神经保护机制仍有待阐明。我们的目的是探讨大黄素的神经保护作用及其可能的机制。在我们的研究中，在人神经母细胞瘤 SH-SY5Y 细胞用高剂量 NaF 处理 24 小时后，检测了突触蛋白和氧化应激损伤。此外，用大黄素预处理以阐明在 NaF 诱导的 SH-SY5Y 细胞毒性中的神经保护作用。我们发现 NaF 显著降低了 SH-SY5Y 细胞中 SNAP 25、突触小泡蛋白和 PSD 95 的蛋白表达。此外，NaF 暴露增加了 p-ERK1/2 的蛋白表达，降低了 Nrf2 和 HO-1 的蛋白表达，并促进了 ROS、4-羟壬烯醛（4-HNE）和 8-羟基-2'-脱氧鸟苷（8-OHdG）的增加。用大黄素预处理可显著恢复 NaF 引起的这些变化。这些数据表明大黄素具有神经保护作用，并指出其在预防氟化物诱导的神经毒性方面具有广阔的应用前景。
