Inhibitory Effects of Myricetin on Lipopolysaccharide-Induced Neuroinflammation
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Published on: August 23, 2022
Jung-Hee Jang1,2, Seung Hoon Lee3, Kyungsook Jung4
1Department of Neurologic Disorders & Aging Brain Constitution, Dunsan Korean Medicine Hospital, Daejeon 34054, Korea.
Abstract:
Microglial activation elicits an immune response by producing proinflammatory modulators and cytokines that cause neurodegeneration. Therefore, a plausible strategy to prevent neurodegeneration is to inhibit neuroinflammation caused by microglial activation. Myricetin, a natural flavanol, induces neuroprotective effects by inhibiting inflammation and oxidative stress. However, whether myricetin inhibits lipopolysaccharide (LPS)-induced neuroinflammation in hippocampus and cortex regions is not known. To test this, we examined the effects of myricetin on LPS-induced neuroinflammation in a microglial BV2 cell line. We found that myricetin significantly downregulated several markers of the neuroinflammatory response in LPS-induced activated microglia, including inducible nitric oxide (NO) synthase (iNOS), cyclooxygenase-2 (COX-2), and proinflammatory modulators and cytokines such as prostaglandin E2 (PGE2), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α). Moreover, myricetin suppressed the expression of c-Jun NH2-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK), which are components of the mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, myricetin inhibited LPS-induced macrophages and microglial activation in the hippocampus and cortex of mice. Based on our results, we suggest that myricetin inhibits neuroinflammation in BV2 microglia by inhibiting the MAPK signaling pathway and the production of proinflammatory modulators and cytokines. Therefore, this could potentially be used for the treatment of neuroinflammatory diseases.
Insights
Myricetin, a natural compound, effectively reduces neuroinflammation by inhibiting key inflammatory markers and pathways in microglial cells. This suggests its potential for treating neuroinflammatory diseases.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglial activation drives neuroinflammation and neurodegeneration through proinflammatory mediators.
- Inhibiting microglial activation is a potential therapeutic strategy for neurodegenerative diseases.
- Myricetin exhibits known anti-inflammatory and antioxidant properties, suggesting neuroprotective potential.
Purpose of the Study:
- To investigate the efficacy of myricetin in inhibiting lipopolysaccharide (LPS)-induced neuroinflammation in microglial cells and mouse models.
- To elucidate the molecular mechanisms underlying myricetin's anti-neuroinflammatory effects.
Main Methods:
- Utilized BV2 microglial cell line stimulated with LPS.
- Assessed the expression of neuroinflammatory markers (iNOS, COX-2, PGE2, IL-1β, TNF-α).
- Examined the involvement of the mitogen-activated protein kinase (MAPK) signaling pathway (JNK, p38, ERK).
- Evaluated myricetin's effects on microglial activation in the hippocampus and cortex of mice.
Main Results:
- Myricetin significantly downregulated key neuroinflammatory markers in LPS-activated microglia.
- Myricetin suppressed the activation of MAPK signaling pathways (JNK, p38, ERK).
- Myricetin inhibited LPS-induced microglial activation in both cell cultures and mouse brain regions.
Conclusions:
- Myricetin effectively inhibits LPS-induced neuroinflammation in microglial cells.
- The mechanism involves the suppression of the MAPK signaling pathway and proinflammatory cytokine production.
- Myricetin shows promise as a therapeutic agent for neuroinflammatory diseases.
