The liquid Panax ginseng inhibits epidermal growth factor-induced metalloproteinase 9 and cyclooxygenase 2 expressions via inhibition of inhibitor factor kappa-B-alpha and extracellular signal-regulated kinase in NCI-H292 human airway epithelial cells

被引:6
作者
Kim, Jung-Hee [1 ]
Kang, Jeong Woo [1 ]
Kim, ManSub [1 ]
Lee, Dong Hun [1 ]
Kim, Heejong [1 ]
Choi, Hee-Sook [1 ]
Kim, Eun Jin [1 ]
Chung, Ill-Min [2 ]
Chung, Il-Yup [3 ]
Yoon, Do-Young [1 ]
机构
[1] Konkuk Univ, Dept Biosci & Biotechnol, Bio Mol Informat Ctr, Seoul 143701, South Korea
[2] Konkuk Univ, Dept Appl Life Sci, Seoul 143701, South Korea
[3] Hanyang Univ, Coll Sci & Technol, Div Mol & Life Sci, Ansan, South Korea
基金
新加坡国家研究基金会;
关键词
NECROSIS-FACTOR-ALPHA; FACTOR RECEPTOR ACTIVATION; MUCIN PRODUCTION; TYROSINE KINASE; MURINE MODEL; CANCER-CELLS; TNF-ALPHA; PROTEIN; MATRIX-METALLOPROTEINASE-9; PATHWAY;
D O I
10.2500/ajra.2011.25.3586
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
Background: Ginseng (Panax ginseng C. A. Meyer) has been used in Asian countries for the treatment of various diseases. However, the mechanisms of liquid Panax ginseng (LG) on allergic inflammatory response in epidermal growth factor (EGF)-stimulated human airway epithelial cells remain largely unclear. Methods: MUC5AC, cyclooxygenase (COX) 2, and matrix metalloproteinase (MMP) 9 expressions were measured using reverse transcription-polymerase chain reaction, Western blotting, and gelatin zymogram analyses in NCI-H292 cells. Extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) protein levels were analyzed by Western blotting. Results: To gain insight into the antiallergy effects of LG, we examined its influence on epidermal growth factor (EGF)-induced MMP-9 and COX-2 productions in NCI-H292 cells. LG was treated for 1 hour and then followed by EGF treatment for 24 hours into NCI-H292 cells. The decrease of COX-2 production was correlated with the reduced levels of proteins and mRNAs of inducible MMP-9 and MUC5AC. LG blocked upstream signaling of NF-kappa-B activation via inhibition of phosphorylations of inhibitor factor-kappa-B-alpha (I-kappa-B-alpha) and ERK. These results suggest that LG protects NCI-H292 cells from EGF-induced damage by down-regulation of COX-2, MMP-9, and MUC5AC gene expressions by blocking NF-kappa-B and ERK. Conclusion: LG modulates allergic inflammatory response in EGF-stimulated NCI-H292 human airway epithelial cells via inhibition of I-kappa-B-alpha and ERK. (Am J Rhinol Allergy 25, e55-e59, 2011; doi: 10.2500/ajra.2011.25.3586)
引用
收藏
页码:E55 / E59
页数:5
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