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At present, the mechanism of fluorosis-induced damage to the hepatic system is unclear. Studies have shown that excess fluoride causes some degree of damage to the liver, including inflammation. The SDF-1/CXCR4 signaling axis has been reported to have an impact on the regulation of inflammation in human cells. In this study, we investigated the role of the SDF-1/CXCR4 signaling axis and related inflammatory factors in fluorosis through in vitro experiments on human hepatic astrocytes (LX-2) cultured with sodium fluoride. CCK-8 assays showed that the median lethal dose at 24 h was 2 mmol/l NaF, and these conditions were used for subsequent enzyme-linked immunosorbent assays (ELISAs) and quantitative real-time polymerase chain reaction (qPCR) analysis. The protein expression levels of SDF-1/CXCR4 and the related inflammatory factors nuclear factor-κB (NF-κB), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) were detected by ELISAs from the experimental and control groups. The mRNA expression levels of these inflammatory indicators were also determined by qPCR in both groups. Moreover, the expression levels of these factors were significantly higher in the experimental group than in the control group at both the protein and mRNA levels (P < 0.05). Excess fluorine may stimulate the SDF-1/CXCR4 signaling axis, activating the inflammatory NF-κB signaling pathway and increasing the expression levels of the related inflammatory factors IL-6, TNF-α and IL-1β. Identification of this mechanism is important for elucidating the pathogenesis of fluorosis-induced liver injury.

目前，氟中毒引发肝脏系统损伤的具体机制尚不明确。已有研究表明，过量氟会对肝脏造成一定程度的损伤，包括炎症反应。基质细胞衍生因子1/CXC趋化因子受体4（SDF-1/CXCR4）信号轴已被证实可调控人体细胞内的炎症反应。本研究通过使用氟化钠培养人肝星形细胞（LX-2）的体外实验，探究了SDF-1/CXCR4信号轴及相关炎症因子在氟中毒中的作用。细胞计数试剂盒-8（Cell Counting Kit-8，CCK-8）实验结果显示，24小时半数致死剂量的氟化钠浓度为2 mmol/L，后续的酶联免疫吸附实验（ELISA）与实时荧光定量聚合酶链反应（qPCR）分析均采用该处理条件。通过ELISA分别检测实验组与对照组中SDF-1/CXCR4及相关炎症因子核因子κB（NF-κB）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）与白细胞介素1β（IL-1β）的蛋白表达水平。两组样本中上述炎症指标的mRNA表达水平亦通过qPCR进行了检测。此外，实验组上述因子在蛋白与mRNA水平的表达量均显著高于对照组（P < 0.05）。过量氟可能通过激活SDF-1/CXCR4信号轴，进而活化炎症相关的NF-κB信号通路，并上调相关炎症因子IL-6、TNF-α与IL-1β的表达水平。阐明该机制对于解析氟中毒引发肝损伤的发病机制具有重要意义。