JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells
Open accessAbstract
Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS have been characterized as an important secondary messenger and modulator for various mammalian intracellular signaling pathways, including the MAPK pathways. In this study we examined ROS production and TNF- α , IL-1 β inflammatory cytokines releasing, and the expression of MAPKs in BV-2 microglia cells treated with fluoride. We found that fluoride increased JNK phosphorylation level of BV-2 cells and pretreatment with JNK inhibitor SP600125 markedly reduced the levels of intracellular O₂(·-) and NO. NOX inhibitor apocynin and iNOS inhibitor SMT dramatically decreased NaF-induced ROS and NO generations, respectively. Antioxidant melatonin (MEL) resulted in a reduction in JNK phosphorylation in fluoride-stimulated BV-2 microglia. The results confirmed that NOX and iNOS played an important role in fluoride inducing oxidative stress and NO production and JNK took part in the oxidative stress induced by fluoride and meanwhile also could be activated by ROS in fluoride-treated BV-2 cells.
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ROS may contribute to microglial activation via p38 and JNK activation.
“ROS may contribute to microglial activation via p38 and JNK activation.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [154]
Attenuating fluoride-induced oxidative stress in BV-2 microglia with the antioxidant melatonin results in reduced JNK activation.
“Attenuating fluoride-induced oxidative stress in BV-2 microglia with the antioxidant, melatonin, results in reduced JNK activation [154].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [154]
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- Authors
- Yan, L., Liu, S., Wang, C., Wang, F., Song, Y., Yan, N., Xi, S., Liu, Z., & Sun, G.
- Affiliations
- China Medical University (CN)
- Corresponding author
- Xi, Shuhua
- Venue
- Mediators of Inflammation
- Publisher
- Hindawi Limited
- Published
- 2013
- Volume
- 2013
- Pages
- 1-10
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC3773420
- OpenAlex
- W2036762936
- Cited by
- 58
- References
- 43
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 1 · 2020: 7 · 2019: 1 · 2018: 8 · 2017: 4 · 2016: 5 · 2015: 5 · 2014: 6
- FWCI
- 4.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministry of Education, Science and Technology
- Science and Technology Development Center, Ministry of Education (20112104110021)
- Topics
- Physical Sciences › Environmental Science › Water Science and Technology › Fluoride Effects and Removal
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- fluoride toxicity, oxidative stress, microglia, NADPH oxidase, JNK, reactive oxygen species, nitric oxide, inducible nitric oxide synthase, MAPK signaling, TNF-α, IL-1β, melatonin, SP600125, apocynin, sodium fluoride, neuroinflammation
- MeSH terms
- Acetophenones, Animals, Anthracenes, Antioxidants, Cell Line, Cell Survival, Enzyme Inhibitors, Enzyme-Linked Immunosorbent Assay, Fluorides, Inflammation, Melatonin, Nitric Oxide, Oxygen, Phosphorylation, Gene Expression Regulation, Enzymologic, Reactive Oxygen Species, Microglia, Oxidative Stress, NADPH Oxidases, MAP Kinase Kinase 4, Mice, Nitric Oxide Synthase Type II
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