Anti-Inflammatory Effects of Ginsenoside Rg3 via NF-<i>κ</i>B Pathway in A549 Cells and Human Asthmatic Lung Tissue

Abstract

<i>Objective</i>. There is limited information of the anti-inflammatory effects of Rg3 on inflamed lung cells and tissues. Therefore, we confirmed the anti-inflammatory mechanism of ginsenoside Rg3 in inflamed human airway epithelial cells (A549) and tissues whether Rg3 regulates nuclear factor kappa B (NF-<i>κ</i>B) activity. <i>Methods</i>. To induce the inflammation, IL-1<i>β</i> (10 ng/ml) was treated to A549 cells for 4 h. The effects of Rg3 on NF-<i>κ</i>B activity and COX-2 expression were evaluated by western blotting analysis in both IL-1<i>β</i>-induced inflamed A549 cell and human asthmatic airway epithelial tissues. Using multiplex cytokines assay, the secretion levels of NF-<i>κ</i>B-mediated cytokines/chemokines were measured. <i>Result</i>. Rg3 showed the significant inhibition of NF-<i>κ</i>B activity thereby reduced COX-2 expression was determined in both IL-1<i>β</i>-induced inflamed A549 cell and human asthmatic airway epithelial tissues. In addition, among NF-<i>κ</i>B-mediated cytokines, the secretion levels of IL-4, TNF-<i>α</i>, and eotaxin were significantly decreased by Rg3 in asthma tissues. Even though there was no significant difference, IL-6, IL-9, and IL-13 secretion showed a lower tendency compared to saline-treated human asthmatic airway epithelial tissues. <i>Conclusion</i>. The results from this study demonstrate the potential of Rg3 as an anti-inflammatory agent through regulating NF-<i>κ</i>B activity and reducing the secretion of NF-<i>κ</i>B-mediated cytokines/chemokines.