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Dietary Polyphenols Decrease Chemokine Release by Human Primary Astrocytes Responding to Pro-Inflammatory Cytokines.

Mikolaj Grabarczyk1, Dominika Ksiazek-Winiarek1, Andrzej Glabinski1

  • 1Department of Neurology and Stroke, Medical University of Lodz, ul. Zeromskiego 113, 90-549 Lodz, Poland.

Pharmaceutics
|September 28, 2023
PubMed
Summary

Myricetin and chrysin, polyphenols, reduced inflammatory chemokine release in reactive astrocytes without impacting cell viability. These compounds did not exhibit antioxidant effects in the astrocyte cultures.

Keywords:
astrocyteschemokineschrysindietary polyphenolsinflammationmyricetin

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Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Astrocytes are the most abundant glial cells in the central nervous system, crucial for neuronal support and inflammation regulation.
  • Polyphenolic compounds are explored for their therapeutic potential, but their specific anti-inflammatory effects on astrocytes are not fully understood.
  • Chemokines play a significant role in neuroinflammation, making astrocyte-derived chemokines potential therapeutic targets.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of myricetin and chrysin on reactive human astrocytes.
  • To determine if these polyphenols can modulate chemokine release from astrocytes stimulated with pro-inflammatory cytokines.
  • To assess the antioxidant properties of myricetin and chrysin in astrocyte cultures.

Main Methods:

  • Primary human astrocytes were cultured and induced to a reactive state using a cytokine mixture (TNF-α, IL-1a, C1q).
  • The effects of myricetin and chrysin on chemokine secretion (CCL5, CCL1, CCL2) were measured.
  • Cell viability was assessed to ensure safety of the tested compounds.
  • Antioxidant potential was evaluated in the astrocyte cultures.

Main Results:

  • Myricetin and chrysin significantly altered the secretion of specific chemokines by reactive astrocytes.
  • Chrysin notably reduced CCL5 release, while myricetin decreased CCL1 release.
  • Both myricetin and chrysin reduced CCL2 secretion.
  • No significant antioxidant activity was observed for either compound in this astrocyte model.
  • Cell viability remained unaffected by the tested concentrations of myricetin and chrysin.

Conclusions:

  • Myricetin and chrysin demonstrate potential as modulators of neuroinflammation by reducing chemokine release from reactive astrocytes.
  • These findings highlight the specific anti-inflammatory actions of these polyphenols on astrocytes, independent of antioxidant effects.
  • Further research into myricetin and chrysin could lead to novel therapeutic strategies for neuroinflammatory conditions targeting astrocyte pathways.