Protection of Resveratrol (RSV) against the neurotoxicity induced by high level of fluoride was investigated. Sprague-Dawley (SD) rats and their offspring, as well as cultures of primary neurons were divided randomly into four groups: untreated (control); treated with 50 mg RSV/kg/ (once daily by gavage) or (20 M in the cultured medium); exposed to 50 ppm F- in drinking water or 4 mmol/l in the cultured medium; and exposed to fluoride then RSV as above. The adult rats were treated for 7 months and the offspring sacrificed at 28 days of age; the cultured neurons for 48 hr. For general characterization, dental fluorosis was assessed and the fluoride content of the urine measured (by fluoride-electrode) in the rates and the survival of cultured neurons monitored with the CCK-8 test. The spatial learning and memory of rats were assessed with the Morris water maze test. The levels of α7 and α4 nicotinic acetylcholine receptors (nAChRs) were quantified by Western blotting; and the activities of superoxide dismutase (SOD) and catalase (CAT), and the levels of malondialdehyde (MDA) and H₂O₂ assayed biochemically. The results showed that chronic fluorosis resulted in the impaired learning and memory in rats and their offspring, and more oxidative stress in both rat brains and cultured neurons, which may be associated the lower levels of α7 and α4 nAChR subunits. Interestingly, RSV attenuated all of these toxic effects by fluorosis, indicating that protection against the neurotoxicity of fluoride by RSV might be in mechanism involved enhancing the expressions of these nAChRs.

研究了白藜芦醇（RSV）对高水平氟化物诱导的神经毒性的保护作用。将Sprague-Dawley（SD）大鼠及其后代以及原代神经元培养物随机分为四组：未治疗（对照组）；未治疗 用50 mg RSV / kg /（每天一次通过管饲法）或（在培养基中20 M）处理 在饮用水中暴露于50 ppm F-或在培养基中暴露于4 mmol / l；然后暴露于氟化物中，然后如上所述暴露于RSV中。成年大鼠接受治疗7个月，后代在28日龄被处死。培养的神经元持续48小时。对于一般特征，评估了氟中毒，并通过CCK-8测试监测了尿液中氟的含量（通过氟电极）和培养的神经元的存活率。用莫里斯水迷宫测试评估大鼠的空间学习和记忆。通过Western印迹定量测定α7和α4烟碱乙酰胆碱受体（nAChRs）的水平。超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，丙二醛（MDA）和H的水平生化分析₂ O ₂。结果表明，慢性氟中毒导致大鼠及其后代的学习和记忆受损，大鼠脑和培养的神经元均遭受更多的氧化应激，这可能与较低的α7和α4nAChR亚基水平有关。有趣的是，RSV通过氟中毒减弱了所有这些毒性作用，表明RSV对氟对神经毒性的保护作用可能与增强这些nAChRs的表达有关。