Delphinidin Inhibits LPS-Induced MUC8 and MUC5B Expression Through Toll-like Receptor 4-Mediated ERK1/2 and p38 MAPK in Human Airway Epithelial Cells.
- Author:
Chang Hoon BAE
1
;
Bo Sung JEON
;
Yoon Seok CHOI
;
Si Youn SONG
;
Yong Dae KIM
Author Information
- Publication Type:Original Article
- Keywords: Delphinidin; Lipopolysaccharides; Toll-like receptor 4; Human MUC8 protein; Human MUC5B protein; Airway epithelial cell
- MeSH: Anthocyanins; Epithelial Cells*; Gene Expression; Humans; Immunoenzyme Techniques; Lipopolysaccharides; p38 Mitogen-Activated Protein Kinases*; Phosphorylation; Phosphotransferases; Protein Kinases; Real-Time Polymerase Chain Reaction; RNA, Messenger; RNA, Small Interfering; Toll-Like Receptor 4; Toll-Like Receptors*
- From:Clinical and Experimental Otorhinolaryngology 2014;7(3):198-204
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVES: Delphinidin is one of the anthocyanidins. It is believed to have anti-inflammatory property including antioxidant, antiangiogenic, and anti-cancer properties. However, the anti-inflammatory effect of delphinidin in mucin-producing human airway epithelial cells has not been determined. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of delphinidin in lipopolysaccharide (LPS)-induced MUC8 and MUC5B expression in human airway epithelial cells. METHODS: In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay were used for investigating the expressions of MUC8, MUC5, and Toll-like receptor 4 (TLR4), after LPS treatment and delphinidin treatment. And the signaling pathway of delphinidin on LPS-induced MUC8 and MUC5B expression was investigated using the RT-PCR, and immunoblot analysis. To confirm the involvement of TLR4 in LPS-induced MUC8 and MU5B expression, the cells were transfected with TLR4 siRNA. RESULTS: In NCI-H292 airway epithelial cells, LPS (100 ng/mL) significantly induced TLR4, MUC8, and MUC5B expression. TLR4 siRNA significantly blocked LPS-induced MUC8 and MUC5B mRNA expression. LPS (100 ng/mL) significantly activated the phosphorylation of extracellular signal related kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK). Delphinidin (50 and 100 microM) inhibited LPS-induced TLR4, MUC8, and MUC5B expression and LPS-induced phosphorylation of ERK1/2 and p38 MAPK. In the primary cultures of normal nasal epithelial cells, delphinidin (50 and 100 microM) significantly inhibited LPS-induced TLR4, MUC8, and MUC5B gene expression. CONCLUSION: These results suggest that delphinidin attenuates LPS-induced MUC8 and MUC5B expression through the TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. These findings indicated that delphinidin may be a therapeutic agent for control of inflammatory airway diseases.
