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Published on: July 25, 2022
Suppression of LPS-induced inflammatory responses by inflexanin B in BV2 microglial cells
Ji-Youn Lim1, Donggeun Sul, Bang Yeon Hwang
1Environmental Toxico-Genomic & Proteomic Center, College of Medicine, Korea University, Seoul 136-701, Korea.
Abstract:
Microglia are a type of resident macrophage that functions as an inflammation modulator in the central nervous system. Over-activation of microglia by a range of stimuli disrupts the physiological homeostasis of the brain, and induces inflammatory response and degenerative processes, such as those implicated in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Therefore, we investigated the possible anti-inflammatory mechanisms of inflexanin B in murine microglial BV2 cells. Lipopolysaccharide (LPS) activated BV2 cells and induced the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and cytokines (interleukins-1β and -6, and tumour necrosis factor α). The LPS-induced production of pro-inflammatory mediators was associated with the enhancement of nuclear factor-kappaB (NF-κB) nuclear translocation and the activation of mitogen-activated protein kinase (MAPK) including ERK1/2 and JNK. Conversely, pretreatment of cells with inflexanin B (10 and 20 μg/mL) significantly reduced the production of pro-inflammatory mediators. This was accompanied with the reduced nuclear translocation of NF-κB and reduced activation of MAPKs. These results suggest that inflexanin B attenuated the LPS-induced inflammatory process by inhibiting the activation of NF-κB and MAPKs.
Insights
Inflexanin B reduces brain inflammation by inhibiting key signaling pathways in microglia, offering potential for neurodegenerative disease treatment. This study shows inflexanin B calms overactive microglia, crucial for maintaining brain health.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Microglia are key immune cells in the central nervous system, regulating inflammation.
- Over-activated microglia contribute to neuroinflammation and neurodegenerative diseases like Alzheimer's and Parkinson's.
- Understanding microglia modulation is vital for developing treatments for neurological disorders.
Purpose of the Study:
- To investigate the anti-inflammatory effects of inflexanin B on activated murine microglial cells.
- To elucidate the molecular mechanisms by which inflexanin B exerts its anti-inflammatory action.
- To assess inflexanin B's potential in mitigating neuroinflammatory processes.
Main Methods:
- Murine microglial BV2 cells were activated using lipopolysaccharide (LPS).
- The production of pro-inflammatory mediators (NO, PGE2, cytokines) was measured.
- Key signaling pathways, including NF-κB and MAPK (ERK1/2, JNK), were analyzed.
- Cells were pretreated with varying concentrations of inflexanin B before LPS stimulation.
Main Results:
- LPS-induced production of nitric oxide, prostaglandin E2, and pro-inflammatory cytokines was significantly reduced by inflexanin B.
- Inflexanin B inhibited the nuclear translocation of NF-κB.
- Inflexanin B suppressed the activation of MAPK signaling pathways (ERK1/2 and JNK).
Conclusions:
- Inflexanin B demonstrates significant anti-inflammatory properties in LPS-activated microglia.
- The anti-inflammatory effects are mediated through the inhibition of NF-κB and MAPK signaling pathways.
- Inflexanin B holds potential as a therapeutic agent for neuroinflammatory conditions.
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