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Abstract
We speculated that peroxisome proliferator-activated receptor (PPAR)-γ agonists may
modulate the oxidative stress pathway to ameliorate the development of airway inflammation.
The effect of Monascus-fermented metabolite monascin (MS) and rosiglitazone (Rosi)
on oxidative stress-induced lung inflammation was evaluated. Luciferase assay and
DNA binding activity assay were used to point out that MS may be a novel PPAR-γ agonist
and nuclear factor-erythroid 2 related factor 2 (Nrf-2) activator. We used hydrogen
peroxide (H2O2) to induce inflammation in lung epithelial cells. MS and Rosi prevented
H2O2-induced ROS generation in A549 epithelial cells through PPAR-γ translocation,
avoiding inflammatory mediator expression via inhibiting nuclear factor (NF)-κB translocation.
The regulatory ability of MS was abolished by siRNA against PPAR-γ. MS also elevated
antioxidant enzyme expression via Nrf-2 activation. Both PPAR-γ and Nrf-2 might have
benefits against lung inflammation. MS regulated PPAR-γ and Nrf-2 to improve lung
oxidative inflammation.
[1
]Department of Biochemical Science and Technology, College of Life Science, National
Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan