The data of study about the chitosan-selenium nanoparticles on depression-like behaviour induced by fluoride in mice via JAK2-STAT3 pathway

Data 18 firstly showed an unprecedented and very important finding was that 150 mg/L Sodium fluoride (NaF) resulted in the insufficient Se content in cortex. However, CS-SeNPs supplementation was beneficial to cortical Se retention in a dose-dependent manner and could antagonize fluoride-induced cortical Se depletion in data 18, which implied that oral administration of CS-SeNPs could be an effective way to supply Se. Further data 20 and 21 suggested that NaF decreased DA and NE content in the cortex, and 1 mg/kg·bw CS-SeNPs reduced the content of DA and NE, and 2 mg/kg·bw CS-SeNPs reduced the DA levels, while 0.5 mg/kg·bw CS-SeNPs had no obvious impact on the content of DA and NE, suggesting that long-term intake of 1, and 2 mg/kg·bw CS-SeNPs had potential negative effects on the monoamine nervous system. Interestingly, data 20 and 21 demonstrated that 0.5 and 1 mg/kg·bw CS-SeNPs protected against dopaminergic and noradrenergic damage caused by NaF in the cortex of mice in this research, which provided the theoretical basis for CS-SeNPs to exert antidepressant - like behavior. Raw data 22-24 showed that the decreased CORT secretion was induced by fluoride in the cortex, however, the expression of GR was significantly increased in the cortex exposed to fluoride, and there was no obvious change of CRF. 0.5 mg/kg·bw and 2 mg/kg·bw CS-SeNPs significantly increased the secretion of CORT and CRF, and 0.5 mg/kg·bw CS-SeNPs significantly decreased the expression of GR, suggesting that CS-SeNPs may improve the response of HPA axis to stress. What’s more, CS-SeNPs of 0.5 mg/kg·bw, 1 mg/kg·bw and 2 mg/kg·bw reestablished the fluoride-reduced CORT secretion. These results demonstrated that the mechanisms of fluoride-induced depression-like behavior were mainly related to the abnormal secretion of monoamine neurotransmitters, rather than the abnormal hyperactivity of the HPA axis. And 0.5 mg/kg·bw and 1 mg/kg·bw CS-SeNPs reversed the abnormal secretion of monoamine neurotransmitters. These data can be used for reference or comparison to further understand the neurotoxicity of long-term use of CS-SeNPs. At the same time, these data provide a comparison of the neurotoxicity of different doses of CS-SeNPs. 0.5 mg/kg·bw provides a relatively safe threshold for long-term consumption CS-SeNPs.数据集18首次揭示了一项前所未有的重要发现：150 mg/L的氟化钠（Sodium fluoride, NaF）会导致小鼠大脑皮层硒元素含量不足。而补充壳聚糖硒纳米颗粒（CS-SeNPs）可呈剂量依赖性地促进皮层硒元素保留，并能拮抗氟化钠诱导的皮层硒耗竭，这提示口服CS-SeNPs或许是补充硒元素的有效途径。 进一步的数据集20与21显示，氟化钠会降低小鼠皮层内多巴胺（Dopamine, DA）与去甲肾上腺素（Norepinephrine, NE）的含量；1 mg/kg体重的CS-SeNPs可降低这两种递质的含量，2 mg/kg体重的CS-SeNPs可降低多巴胺水平，而0.5 mg/kg体重的CS-SeNPs对二者含量无明显影响，这提示长期摄入1、2 mg/kg体重的CS-SeNPs可能对单胺能神经系统产生潜在负面影响。 有趣的是，数据集20与21证实，本研究中0.5、1 mg/kg体重的CS-SeNPs可拮抗氟化钠诱导的小鼠皮层多巴胺能与去甲肾上腺素能神经损伤，这为CS-SeNPs发挥类抗抑郁行为提供了理论依据。 原始数据集22-24显示，氟化钠可降低小鼠皮层的皮质酮（Corticosterone, CORT）分泌；但暴露于氟化钠的皮层中，糖皮质激素受体（Glucocorticoid Receptor, GR）的表达显著上调，而促肾上腺皮质激素释放因子（Corticotropin-Releasing Factor, CRF）的水平无明显变化。0.5、2 mg/kg体重的CS-SeNPs可显著提升皮质酮与促肾上腺皮质激素释放因子的分泌水平，且0.5 mg/kg体重的CS-SeNPs可显著下调糖皮质激素受体的表达，这提示CS-SeNPs或许可改善下丘脑-垂体-肾上腺轴（Hypothalamic-Pituitary-Adrenal axis, HPA轴）对应激的应答能力。此外，0.5、1、2 mg/kg体重的CS-SeNPs均可恢复氟化钠降低的皮质酮分泌水平。 上述结果表明，氟化钠诱导的类抑郁行为机制主要与单胺类神经递质分泌异常相关，而非下丘脑-垂体-肾上腺轴的过度激活；且0.5、1 mg/kg体重的CS-SeNPs可逆转单胺类神经递质的分泌异常。 本数据集可用于参考或对比，以进一步明确长期使用CS-SeNPs的神经毒性；同时，这些数据也为不同剂量CS-SeNPs的神经毒性对比提供了依据。其中0.5 mg/kg体重可为长期摄入CS-SeNPs提供相对安全的剂量阈值。