Abstract

After the establishment of fluorosis animal model, the gene expression of SNAP-25 was detected in order to provide experimental data for nervous system injury induced by fluoride. The results showed that, compared with the de-ionized water group, SNAP-25 mRNA expression was significantly reduced by fluoride.

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    Introduction: Curcumin, a yellow-pigment, found in the popular Indian spice turmeric (Curcuma longa), poses pharmaceutical applications due to its anti-inflammatory, antioxidant, and chemoprotective properties. Excessive fluoride causes fluorosis leading to neurodegeneration and associated behavioral deficits, particularly in children. This study aimed at investigating the neuroprotective ability of curcumin on sodium

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    Objective: To investigate the expression and distribution of the downstream substrate of extracellular regulated protein kinase(ERK1/2) pathway, ternary complex factor phospho-Elk-1, in rat brains with chronic fluorosis, and reveal the mechanism of the impaired learning and memory ability caused by chronic fluorosis. Methods: Seventy-two SD rats, weighing 100 - 120 g,

  • Changed expressions of N-methyl-D-aspartate receptors in the brains of rats and primary neurons exposed to high level of fluoride

    Expressions of N-methyl-d-aspartic acid receptors (NMDARs) in the brains of rats and primary neurons exposed to high fluoride were investigated. Sprague-Dawley rats were divided randomly into a fluorosis group (50 ppm fluoride in the drinking water for 6 months) and controls (<0.5ppm fluoride) and the offspring from these rats sacrificed

  • MiR-132, miR-204 and BDNF-TrkB signaling pathway may be involved in spatial learning and memory.

    Highlights Spatial learning and memory of offspring rats were impaired after exposure to fluorine combined with aluminium(FA). Hippocampal miR-132 and miR-204 were increased after FA exposure. Hippocampal BDNF-TrkB signaling pathway was down-regulated after FA exposure. There were antagonistic effects between F and Al, with Al reducing the toxicity of F. Fluorine

  • Roles of mitochondrial fission inhibition in developmental fluoride neurotoxicity: mechanisms of action in vitro and associations with cognition in rats and children.

    Fluoride neurotoxicity is associated with mitochondrial disruption. Mitochondrial fission/fusion dynamics is crucial to maintain functional mitochondria, yet little is known about how fluoride perturbs this dynamics and whether such perturbation contributes to impaired neurodevelopment. Here in human neuroblastoma SH-SY5Y cells treated with sodium fluoride (NaF, 20, 40 and 60 mg/L), mitochondrial

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