Monascin attenuates oxidative stress-mediated lung inflammation via peroxisome proliferator-activated receptor-gamma (PPAR-γ) and nuclear factor-erythroid 2 related factor 2 (Nrf-2) modulation.

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.

• Authors: Wei-Hsuan Hsu, Bao-Hong Lee, Tzu-Ming Pan
• Journal: Journal of agricultural and food chemistry (J Agric Food Chem) Vol. 62 Issue 23 Pg. 5337-44 (Jun 11 2014) ISSN: 1520-5118 [Electronic] United States
• PMID: 24865672 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Heterocyclic Compounds, 3-Ring
• NF-E2-Related Factor 2
• PPAR gamma
• monascin

Topics

• Cell Line
• Heterocyclic Compounds, 3-Ring (metabolism, pharmacology)
• Humans
• Monascus (chemistry, metabolism)
• NF-E2-Related Factor 2 (genetics, immunology)
• Oxidative Stress (drug effects)
• PPAR gamma (genetics, immunology)
• Pneumonia (drug therapy, genetics, immunology, metabolism)