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Aquilariae Lignum Methylene Chloride Fraction Attenuates IL-1β-Driven Neuroinflammation in BV2 Microglial Cells
Jin-Seok Lee1, Yoo-Jin Jeon1, Ji-Yun Kang1
1Institute of Bioscience & Integrative Medicine, Dunsan Hospital of Daejeon University, Daejeon 35235, Korea.
Abstract:
Microglial hyperactivation and neuroinflammation are known to induce neuronal death, which is one of the main causes of neurodegenerative disorders. We previously found that Aquilariae Lignum extract attenuated both neuronal excitotoxicity and neuroinflammation in vivo and in vitro. For further analysis, we extracted the methylene chloride fraction of Aquilariae Lignum to determine the bioactive compounds. In this study, we investigated the anti-neuroinflammatory effects and underlying mechanisms of the Aquilariae Lignum fraction (ALF) using lipopolysaccharide (LPS)-stimulated BV2 microglial cells. BV2 cells were pretreated with ALF (0.5, 1, and 2.5 μg/mL) before treatment with LPS (1 μg/mL). Pretreatment with ALF significantly attenuated the LPS-induced overproductions of nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and interleukin (IL)-1β. These anti-inflammatory effects were supported by ALF-mediated modulation of the nuclear factor-kappa B (NF-κB) pathway. Furthermore, ALF exerted strong anti-inflammasome effects, as shown by IL-1β-specific inhibitory activity, but not activity against tumor necrosis factor (TNF)-α, along with inhibition of caspase-1 activity and NACHT, LRR, and PYD domain-containing protein 3 (NLRP3)-related molecules. These results indicate the potent anti-neuroinflammatory activity of ALF and that its underlying mechanism may involve the regulation of NLRP3 inflammasome-derived neuroinflammation in microglial cells.
Insights
Aquilariae Lignum fraction (ALF) reduces neuroinflammation by inhibiting the NLRP3 inflammasome pathway in microglial cells. This finding offers potential therapeutic strategies for neurodegenerative disorders.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Neuroinflammation and microglial hyperactivation contribute to neuronal death in neurodegenerative disorders.
- Previous studies indicated Aquilariae Lignum extract has neuroprotective properties.
- Further investigation into specific fractions is needed to identify bioactive compounds.
Purpose of the Study:
- To investigate the anti-neuroinflammatory effects of the Aquilariae Lignum fraction (ALF).
- To elucidate the underlying mechanisms of ALF's anti-neuroinflammatory activity.
- To evaluate ALF's impact on lipopolysaccharide (LPS)-stimulated BV2 microglial cells.
Main Methods:
- BV2 microglial cells were pretreated with ALF before LPS stimulation.
- Assessed the production of nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and interleukin-1β (IL-1β).
- Investigated the modulation of nuclear factor-kappa B (NF-κB) and NLRP3 inflammasome components (caspase-1, NLRP3).
Main Results:
- ALF significantly attenuated LPS-induced overproduction of NO, COX-2, PGE2, and IL-1β.
- ALF demonstrated anti-inflammasome activity by inhibiting caspase-1 and NLRP3-related molecules.
- ALF modulated the NF-κB pathway, contributing to its anti-inflammatory effects.
Conclusions:
- The Aquilariae Lignum fraction (ALF) possesses potent anti-neuroinflammatory activity.
- ALF's mechanism involves the regulation of NLRP3 inflammasome-mediated neuroinflammation in microglial cells.
- ALF shows promise as a therapeutic agent for neurodegenerative diseases.
