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Nordalbergin Exerts Anti-Neuroinflammatory Effects by Attenuating MAPK Signaling Pathway, NLRP3 Inflammasome
Jung Lo1,2, Hsin-En Wu3, Ching-Chih Liu3,4
1Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Abstract:
Microglia-associated neuroinflammation is recognized as a critical factor in the pathogenesis of neurodegenerative diseases; however, there is no effective treatment for the blockage of neurodegenerative disease progression. In this study, the effect of nordalbergin, a coumarin isolated from the wood bark of Dalbergia sissoo, on lipopolysaccharide (LPS)-induced inflammatory responses was investigated using murine microglial BV2 cells. Cell viability was assessed using the MTT assay, whereas nitric oxide (NO) production was analyzed using the Griess reagent. Secretion of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) was detected by the ELISA. The expression of inducible NO synthase (iNOS), cyclooxygenase (COX)-2, mitogen-activated protein kinases (MAPKs) and NLRP3 inflammasome-related proteins was assessed by Western blot. The production of mitochondrial reactive oxygen species (ROS) and intracellular ROS was detected using flow cytometry. Our experimental results indicated that nordalbergin ≤20 µM suppressed NO, IL-6, TNF-α and IL-1β production; decreased iNOS and COX-2 expression; inhibited MAPKs activation; attenuated NLRP3 inflammasome activation; and reduced both intracellular and mitochondrial ROS production by LPS-stimulated BV2 cells in a dose-dependent manner. These results demonstrate that nordalbergin exhibits anti-inflammatory and anti-oxidative activities through inhibiting MAPK signaling pathway, NLRP3 inflammasome activation and ROS production, suggesting that nordalbergin might have the potential to inhibit neurodegenerative disease progression.
Insights
Nordalbergin, a compound from Dalbergia sissoo, reduces inflammation and oxidative stress in microglia. This suggests potential for treating neurodegenerative diseases by inhibiting key inflammatory pathways.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Neuroinflammation driven by microglia is central to neurodegenerative diseases.
- Current treatments lack efficacy in halting disease progression.
- Nordalbergin, a coumarin from Dalbergia sissoo, is investigated for its anti-inflammatory properties.
Purpose of the Study:
- To evaluate the anti-inflammatory and anti-oxidative effects of nordalbergin on lipopolysaccharide (LPS)-induced responses in murine microglial BV2 cells.
- To elucidate the underlying molecular mechanisms, including the involvement of MAPK signaling, NLRP3 inflammasome, and reactive oxygen species (ROS).
Main Methods:
- Cell viability assessed via MTT assay.
- Nitric oxide (NO) production measured by Griess reagent.
- Cytokine secretion (IL-6, TNF-α, IL-1β) quantified using ELISA.
- Protein expression (iNOS, COX-2, MAPKs, NLRP3 inflammasome) analyzed by Western blot.
- Intracellular and mitochondrial ROS levels determined by flow cytometry.
Main Results:
- Nordalbergin (≤20 µM) dose-dependently suppressed LPS-induced NO, IL-6, TNF-α, and IL-1β production.
- It decreased inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) expression.
- Nordalbergin inhibited mitogen-activated protein kinases (MAPKs) activation and NLRP3 inflammasome activation.
- Reduced intracellular and mitochondrial ROS production was observed.
Conclusions:
- Nordalbergin exhibits significant anti-inflammatory and anti-oxidative activities in microglia.
- These effects are mediated by the inhibition of MAPK signaling, NLRP3 inflammasome activation, and ROS production.
- Nordalbergin shows potential as a therapeutic agent for neurodegenerative diseases.
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