Artemisia gmelinii Extract Attenuates Particulate Matter-Induced Neutrophilic Inflammation in a Mouse Model of Lung

Hyeon-Ji Song1,2, Dong-Uk Shin1,3, Ji-Eun Eom1

  • 1Division of Food Functionality Research, Korea Food Research Institute (KFRI), Wanju 55365, Republic of Korea.

PubMed

Insights

Artemisia gmelinii extract (AGE) reduces lung inflammation caused by particulate matter (PM). AGE suppresses inflammatory pathways and promotes protective ones, offering a potential treatment for PM-induced respiratory issues.

Area of Science:

  • Environmental Health
  • Pharmacology
  • Respiratory Medicine

Background:

  • Particulate matter (PM) exposure causes oxidative stress and inflammation, leading to respiratory diseases.
  • Artemisia gmelinii extract (AGE) possesses known antioxidant and anti-inflammatory properties.
  • The effect of AGE on PM-induced lung inflammation has not been previously reported.

Purpose of the Study:

  • To investigate the protective effects of AGE in a mouse model of PM-induced lung inflammation.
  • To elucidate the molecular mechanisms underlying AGE's action on inflammatory pathways.

Main Methods:

  • Utilized a PM-induced mouse lung inflammation model.
  • Assessed inflammatory cell counts, chemokine expression, and neutrophil extracellular trap (NET) formation in bronchoalveolar lavage fluid (BALF).
  • Analyzed the modulation of NF-κB/MAPK and NRF2/HO-1 signaling pathways in lung tissues and differentiated HL-60 cells.

Main Results:

  • AGE significantly reduced inflammatory cell infiltration, NET formation, and chemokine expression in BALF.
  • AGE suppressed the NF-κB/MAPK signaling pathway while activating the NRF2/HO-1 pathway in lung tissues.
  • AGE decreased inflammatory cytokines, chemokines, reactive oxygen species, and key enzymes like myeloperoxidase and neutrophil elastase in vitro.

Conclusions:

  • AGE effectively suppresses PM-induced lung inflammation, neutrophil infiltration, and tissue damage.
  • The protective effects are mediated by the inhibition of NF-κB/MAPK signaling and the enhancement of NRF2/HO-1 signaling.
  • AGE demonstrates potential as a therapeutic agent for preventing and treating particulate matter-induced respiratory inflammation.

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