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@ARTICLE{Owona:276280,
      author       = {Owona, Brice Ayissi and Mary, Arnaud and Messi, Angelique N
                      and Ravichandran, Kishore Aravind and Mbing, Josephine Ngo
                      and Pegnyemb, Emmanuel and Moundipa, Paul F and Heneka,
                      Michael},
      title        = {{B}iflavonoid {M}ethylchamaejasmin and {K}haya
                      grandifoliola {E}xtract {I}nhibit {NLRP}3 {I}nflammasome in
                      {THP}-1 {C}ell {M}odel of {N}euroinflammation.},
      journal      = {Molecular neurobiology},
      volume       = {62},
      number       = {2},
      issn         = {0893-7648},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {DZNE-2025-00259},
      pages        = {1605 - 1619},
      year         = {2025},
      abstract     = {Neuroinflammation is a common hallmark of Alzheimer's
                      disease (AD), with NLRP3 inflammasome proven to be activated
                      in microglia of AD patients' brains. In this study, a newly
                      isolated biflavonoid (7,7'-di-O-methylchamaejasmin/M8) and a
                      crude extract of the plant Khaya grandifoliola (KG) were
                      investigated for their inhibitory effect on inflammasome
                      activation. In preliminary experiments, M8 and KG showed no
                      cytotoxicity on human macrophage-like differentiated THP-1
                      cells and exhibited anti-inflammatory inhibition of nitric
                      oxide produced following lipopolysaccharide stimulation.
                      Furthermore, M8 and KG blocked IL-1β and IL-18 production
                      by reducing NLRP3 inflammasome components including NFκB,
                      NLRP3, Caspase-1, pro-IL-1β, and pro-IL-18 at the mRNA and
                      protein levels. Regarding the formation of ASC
                      (apoptosis-associated speck-like protein containing a CARD)
                      specks during inflammasome activation, the size and
                      fluorescent intensity of the existing specks were unchanged
                      across all treatment conditions. However, M8 and KG
                      treatments were shown to prevent further speck formation. In
                      addition, experiments on amyloid β phagocytosis showed that
                      M8 and KG pretreatments can restore the phagocytic activity
                      of THP-1 cells, which was impaired following inflammasome
                      activation. Altogether, our findings describe for the first
                      time a promising role of biflavonoids and KG extract in
                      preventing inflammasome activation and protecting against
                      neuroinflammation, a key factor in AD development.},
      keywords     = {Humans / NLR Family, Pyrin Domain-Containing 3 Protein:
                      metabolism / Inflammasomes: metabolism / Inflammasomes: drug
                      effects / Plant Extracts: pharmacology / THP-1 Cells /
                      Biflavonoids: pharmacology / Biflavonoids: therapeutic use /
                      Neuroinflammatory Diseases: drug therapy / Neuroinflammatory
                      Diseases: metabolism / Neuroinflammatory Diseases: pathology
                      / Amyloid beta-Peptides: metabolism / Lipopolysaccharides:
                      pharmacology / Meliaceae: chemistry / Phagocytosis: drug
                      effects / Nitric Oxide: metabolism / Interleukin-1beta:
                      metabolism / Khaya grandifoliola (Other) /
                      7,7′-di-O-Methylchamaejasmin (Other) / Biflavonoid (Other)
                      / NLRP3 inflammasome (Other) / THP-1 cells (Other) / NLR
                      Family, Pyrin Domain-Containing 3 Protein (NLM Chemicals) /
                      Inflammasomes (NLM Chemicals) / Plant Extracts (NLM
                      Chemicals) / Biflavonoids (NLM Chemicals) / Amyloid
                      beta-Peptides (NLM Chemicals) / Lipopolysaccharides (NLM
                      Chemicals) / Nitric Oxide (NLM Chemicals) /
                      Interleukin-1beta (NLM Chemicals)},
      cin          = {AG Heneka},
      ddc          = {570},
      cid          = {I:(DE-2719)1011303},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39012444},
      doi          = {10.1007/s12035-024-04365-4},
      url          = {https://pub.dzne.de/record/276280},
}