Aquilariae Lignum Methylene Chloride Fraction Attenuates IL-1β-Driven Neuroinflammation in BV2 Microglial Cells

Autor: Hwa-Dong Lee, Jin-Seok Lee, Samkeun Lee, Chang-Gue Son, Yoo-Jin Jeon, Ji-Yun Kang
Rok vydání: 2020
Předmět:
Lipopolysaccharides
Lipopolysaccharide
Interleukin-1beta
Anti-Inflammatory Agents
Excitotoxicity
microglia
Pharmacology
Nitric Oxide
medicine.disease_cause
Article
Dinoprostone
Catalysis
neuroinflammation
Nitric oxide
lcsh:Chemistry
Inorganic Chemistry
chemistry.chemical_compound
medicine
Animals
Humans
Physical and Theoretical Chemistry
Prostaglandin E2
lcsh:QH301-705.5
Molecular Biology
Spectroscopy
Neuroinflammation
Inflammation
Methylene Chloride
Microglia
Tumor Necrosis Factor-alpha
Organic Chemistry
NF-kappa B
Interleukin
General Medicine
Aquilariae Lignum
NLRP3 inflammasome
Computer Science Applications
medicine.anatomical_structure
Gene Expression Regulation
lcsh:Biology (General)
lcsh:QD1-999
chemistry
Cyclooxygenase 2
Thymelaeaceae
Tumor necrosis factor alpha
Heme Oxygenase-1
Signal Transduction
medicine.drug
Zdroj: International Journal of Molecular Sciences, Vol 21, Iss 5465, p 5465 (2020)
International Journal of Molecular Sciences
Volume 21
Issue 15
ISSN: 1422-0067
DOI: 10.3390/ijms21155465
Popis: 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 &mu
g/mL) before treatment with LPS (1 &mu
g/mL). Pretreatment with ALF significantly attenuated the LPS-induced overproductions of nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and interleukin (IL)-1&beta
These anti-inflammatory effects were supported by ALF-mediated modulation of the nuclear factor-kappa B (NF-&kappa
B) pathway. Furthermore, ALF exerted strong anti-inflammasome effects, as shown by IL-1&beta
specific inhibitory activity, but not activity against tumor necrosis factor (TNF)-&alpha
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.
Databáze: OpenAIRE
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