Protective effect of quercetin on acrolein-induced COX-2 expression in lung epithelial cells

Abstract

The purpose of this study was to determine whether quercetin can protect against acrolein-induced cyclooxygenase-2 (COX-2) expression using rat lung epithelial (LE) cells. The LE cells were exposed to 20 or 60 μM quercetin and 20 μM acrolein for 24 hr. Cell viability was reduced by acrolein, while quercetin 20 μM reduced the adverse effect produced by acrolein. Quercetin alone at 20 μM did not markedly affect cell viability. Acrolein-induced toxicity in LE cells was evidenced by the presence of inflammatory mediators. It was previously reported that exposure of LE cells to 20 μM acrolein produced an upregulation in COX-2 expression that was reduced by 20 μM quercetin. To determine the underlying mechanism of activation of inflammation, the protein expression of NFκB (phosphorylated p65), ERK and MEK, and MAP kinases was determined. These inflammatory mediators were upregulated by acrolein while quercetin reduced the expression of these mediators. Data suggest that quercetin, a flavonoid, may be beneficial in counteracting acrolein-mediated adverse insults to cells via an ERK/MEK/NFκB-mediated inflammatory pathway.

Keywords:

• acrolein
• quercetin
• COX-2
• NFκB

Acknowledgments

Research infrastructure support was provided by grants G12RR003045 and CO6RR012537 awarded by the National Center for Research Resources, National Institutes of Health (NIH). The G12 program is now a part of the National Institute on Minority Health and Health Disparities and the C06 program is in the Office of Research Infrastructure Programs in the Office of the Director, NIH.