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The flavonoid agathisflavone modulates the microglial neuroinflammatory response and enhances remyelination
Monique Marylin Alves de Almeida1, Francesca Pieropan2, Larissa de Mattos Oliveira3
1Department of Biochemistry and Biophysics, Institute of Health Sciences, Federal University of Bahia, Brazil; School of Pharmacy and Biomedical Sciences, University of Portsmouth, United Kingdom.
Abstract:
Myelin loss is the hallmark of the demyelinating disease multiple sclerosis (MS) and plays a significant role in multiple neurodegenerative diseases. A common factor in all neuropathologies is the central role of microglia, the intrinsic immune cells of the central nervous system (CNS). Microglia are activated in pathology and can have both pro- and anti-inflammatory functions. Here, we examined the effects of the flavonoid agathisflavone on microglia and remyelination in the cerebellar slice model following lysolecithin induced demyelination. Notably, agathisflavone enhances remyelination and alters microglial activation state, as determined by their morphology and cytokine profile. Furthermore, these effects of agathisflavone on remyelination and microglial activation were inhibited by blockade of estrogen receptor α. Thus, our results identify agathisflavone as a novel compound that may act via ER to regulate microglial activation and enhance remyelination and repair.
Insights
Agathisflavone, a flavonoid, promotes myelin repair in the central nervous system by modulating microglia activation. This effect is mediated through estrogen receptor alpha, suggesting a new therapeutic avenue for demyelinating diseases like multiple sclerosis.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Myelin loss is a key feature of multiple sclerosis (MS) and other neurodegenerative diseases.
- Microglia, the immune cells of the central nervous system (CNS), play a critical role in neuropathologies, exhibiting both pro- and anti-inflammatory functions.
- Understanding microglial modulation is crucial for developing therapeutic strategies for CNS repair.
Purpose of the Study:
- To investigate the effects of the flavonoid agathisflavone on microglial activation and remyelination.
- To explore the potential role of estrogen receptor alpha (ERα) in mediating agathisflavone's effects on CNS repair.
Main Methods:
- Utilized a cerebellar slice model of demyelination induced by lysolecithin.
- Administered agathisflavone and assessed its impact on remyelination and microglial morphology/cytokine profiles.
- Investigated the role of ERα by blocking its activity and observing the effects on agathisflavone's actions.
Main Results:
- Agathisflavone significantly enhanced remyelination in the demyelinated cerebellar slices.
- Agathisflavone altered microglial activation states, as evidenced by changes in morphology and cytokine production.
- The beneficial effects of agathisflavone on remyelination and microglial activation were attenuated by blockade of estrogen receptor alpha.
Conclusions:
- Agathisflavone is a novel compound that promotes remyelination and modulates microglial activation.
- The mechanism of action for agathisflavone appears to involve estrogen receptor alpha signaling.
- These findings suggest agathisflavone as a potential therapeutic agent for enhancing CNS repair in demyelinating diseases.
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