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.

中文翻译：

---

大黄素通过调节 ERK1/2/Nrf2/HO-1 通路保护 SH-SY5Y 细胞免受氟化物诱导的突触损伤和氧化应激

过量接触氟化物会导致神经毒性作用。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。我们的目的是探索大黄素的神经保护功效和可能的机制。在我们的研究中，在用高剂量 NaF 处理人类神经母细胞瘤 SH-SY5Y 细胞 24 小时后，检查了突触蛋白和氧化应激损伤。此外，使用大黄素预处理来阐明 NaF 诱导的 SH-SY5Y 细胞毒性的神经保护作用。我们发现 NaF 显着降低了 SH-SY5Y 细胞中 SNAP 25、突触素和 PSD 95 的蛋白质表达。此外，NaF 暴露增加了 p-ERK1/2 的蛋白表达并降低了 Nrf2 和 HO-1 的蛋白表达，以及促进增加 ROS、4-羟基壬烯醛 (4-HNE) 和 8-羟基-2'-脱氧鸟苷 (8-OHdG)。用大黄素预处理显着恢复了这些由 NaF 引起的改变。这些数据暗示了大黄素的神经保护作用，并指出了用于预防氟化物引起的神经毒性的有希望的用途。