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Fasudil Attenuates Fluoride-induced Neuronal Synaptic Damage by Inhibiting Microglial Inflammation
Wenjing Yang1, Keming Bu1, Xiaohan Ren1
1Institute for Endemic Fluorosis Control, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang, 150081, China; NHC Key Laboratory of Etiology and Epidemiology (Harbin Medical University), Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health, Key Laboratory of Etiology and Epidemiology,Education Bureau of Heilongjiang Province.
High fluoride exposure harms cognition by activating the RhoA/ROCK pathway, causing neuroinflammation and synaptic damage. A ROCK inhibitor, fasudil, protected against these fluoride-induced effects in rats.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- High fluoride intake is associated with cognitive deficits.
- The precise molecular pathways of fluoride neurotoxicity remain unclear.
Purpose of the Study:
- To investigate if fluoride-induced synaptic damage involves RhoA/ROCK pathway-mediated microglial activation and inflammation.
- To evaluate the therapeutic potential of fasudil, a RhoA/ROCK inhibitor.
Main Methods:
- A subchronic rat model was utilized.
- RhoA/ROCK pathway activation, microglial response, and synaptic injury were assessed.
- The effects of fasudil treatment were examined.
Main Results:
- Fluoride exposure activated the RhoA/ROCK cascade, leading to microglial activation and pro-inflammatory cytokine release.
- Hippocampal synaptic injury was observed following fluoride exposure.
- Fasudil treatment attenuated these effects, reducing Iba1, TNF-α, and ROCK2 expression.
Conclusions:
- RhoA/ROCK signaling is a critical mediator of fluoride-induced neuroinflammation and synaptic damage.
- Targeting the RhoA/ROCK pathway may offer a strategy to mitigate fluoride neurotoxicity.
- These findings provide a mechanistic basis for assessing the neurotoxic risks of environmental fluoride exposure.
