Sesamin Suppresses Macrophage-derived Chemokine Expression in Human Monocytes via Epigenetic Regulation

• Main Authors: Shih-ling Wang, 王詩綾
• Other Authors: David Chao
• Format: Others
• Language: zh-TW
• Published: 2014
• Online Access: http://ndltd.ncl.edu.tw/handle/10048953102455583233

碩士 === 國立中山大學 === 生物科學系研究所 === 102 === Certain chemokines play important roles in asthma. Sesamin has anti-inflammatory effects. Whether sesamin modulates asthma-related chemokines is unknown. We investigated the effects of sesamin on interferon-γ-inducible protein-10 (IP-10/CXCL10), macrophage-derived chemokine (MDC/CCL22), growth-related oncogene-α (GRO-α/CXCL1) and tumor necrosis factor (TNF)-α expression in human monocytes. Cells were pretreated with sesamin and then stimulated with lipopolysaccharide (LPS). IP-10, MDC, GRO-α and TNF-α were measured by ELISA. Mechanisms were investigated by receptor antagonists, pathway inhibitors, Western blotting and chromatin immunoprecipitation. Sesamin suppressed the expression of MDC but had no effects on IP-10, GRO-α and TNF-α expression. The suppressive effect was reversed by the estrogen receptor (ER) and peroxisomal proliferators-activated receptor (PPAR)-α antagonists. Sesamin suppressed phosphorylation of mitogen-activated protein kinase (MAPK)-p38 and nuclear factor κB (NFκB)-p65. Sesamin suppressed histone H3/H4 acetylation in MDC promoter region. Sesamin may suppress asthmatic inflammation by suppressing MDC expression via the ER/PPAR-α, the MAPK-p38 pathway and the NFκB-p65 pathway and the epigenetic regulation.