ArticleFood science and biotechnology2023
Dibenzoylmethane ameliorates adiposity-mediated neuroinflammatory response and inflammation-mediated neuronal cell death in mouse microglia and neuronal cells.
Article in Food science and biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Six promising drug repurposing candidates for Alzheimer's disease and their sex-specific mechanisms and efficacy.Neural regeneration research · 2026Article
- Dibenzoylmethane, a novel β-diketone pore blocker of large-conductance calcium-activated potassium channel.bioRxiv : the preprint server for biology · 2026Article
- Determination of polycyclic aromatic hydrocarbons (PAH4) in licorice root (Food science and biotechnology · 2025Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dibenzoylmethane (DBM), a licorice-derived component, has numerous health benefits. The current study aimed to investigate the effect of DBM on adiposity-induced neuroinflammatory/oxidative response and microglial activation-induced neuronal cell damage. For this research, BV2 and HT22 cells were cultured using adipcyte- and microglia-conditioned media, respectively. DBM effectively suppressed lipopolysaccharide-induced productions in inducible nitric oxide synthase and cyclooxygenase2. Interleukin (IL)-6, monocyte chemoattractant protein-1, IL-1β, and tumor necrosis factor-α levels were also downregulated by DBM. In adipocyte-conditioned medium (ACM)-cultured BV2 cells, DBM effectively decreased ACM-induced generation of nitric oxide, reactive oxygen species, and inflammatory cytokines by activating nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling and reducing nuclear factor kappa-light-chain-enhancer of activated B cells. In BV2-conditioned medium (BVM)-cultured neuron cells, DBM recovered the BVM-induced reduction of neuronal cell viability, thereby regulating B-cell lymphoma 2 (BCL2), BCL2-associated X (BAX), and cleaved caspase-3 protein expression. Taken together, DBM suppressed adiposity-induced inflammation/oxidative responses and inflammation-induced neuronal cell death.
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