4.8 Article

Mitigation Effects of Selenium Nanoparticles on Depression-Like Behavior Induced by Fluoride in Mice via the JAK2-STAT3 Pathway

Journal

ACS APPLIED MATERIALS & INTERFACES
Volume 14, Issue 3, Pages 3685-3700

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acsami.1c18417

Keywords

selenium nanoparticles; fluoride; dopamine; depression-like behavior; microglia; JAK2-STAT3 pathway

Funding

  1. China National Natural Science Foundation [31972751]
  2. Shanxi Province Natural Science Foundation [201901D111230]
  3. Shanxi Province Innovation Project for Graduate Students [2019SY219]
  4. Innovation Projects of the College of Veterinary Medicine, Shanxi Agricultural University [DY-M008]

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This study investigated the effects of selenium nanoparticles on fluoride-induced depression-like behavior. The results showed that selenium nanoparticles can alleviate depression-like symptoms by regulating related signaling pathways and protein expression.
Depression is a mental health problem with typically high levels of distress and dysfunction, and 150 mg/L fluoride (F) can induce depression-like behavior. The development of depression is correlated with neuronal atrophy, insufficient secretion of monoamine neurotransmitters, extreme deviations from the normal microglial activation status, and immune-inflammatory response. Studies found that Se supplementation was related to the improvement of depression. In this study, we applied selenium nanoparticles (SeNPs) for F-induced depression disease mitigation by regulating the histopathology, metabolic index, genes, and protein expression related to the JAK2-STAT3 signaling pathway in vivo. Results showed that F and 2 mg Se/kg BW/day SeNPs lowered the dopamine (DA) content (P < 0.05), altered the microglial morphology, ramification index as well as solidity, and triggered the microglial neuroinflammatory response by increasing the p-STAT3 nuclear translocation (P < 0.01). Furthermore, F reduced the cortical Se content and the number of surviving neurons (P < 0.05), increasing the protein expressions of p-JAK2/JAK2 and p-STAT3/STAT3 of the cortex (P < 0.01), accompanied by the depression-like behavior. Importantly, 1 mg Se/kg BW/day SeNPs alleviated the microglial ramification index as well as solidity changes and decreased the interleukin-1 beta secretion induced by F by suppressing the p-STAT3 nuclear translocation (P < 0.01). Likewise, 1 mg Se/kg BW/day SeNPs restored the F-disturbed dopamine and noradrenaline secretion, increased the number of cortical surviving neurons, and reduced the vacuolation area, ultimately suppressing the occurrence of depression-like behavior through inhibiting the JAK2-STAT3 pathway activation. In conclusion, 1 mg Se/kg BW/day SeNPs have mitigation effects on the F-induced depression-like behavior. The mechanism of how SeNPs repair neural functions will benefit depression mitigation. This study also indicates that inhibiting the JAK/STAT pathway can be a promising novel treatment for depressive disorders.

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