Serum amyloid A promotes the inflammatory response via p38-MAPK/SR-BⅠ pathway in THP-1 macrophages
- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 3
- DOI:
- 10.13294/j.aps.2016.0029
- Key Word:
- B类Ⅰ型清道夫受体;血清淀粉样蛋白A;p38丝裂原活化蛋白激酶;动脉粥样硬化;scavenger receptor class B type Ⅰ;serum amyloid protein A;p38-MAPK;atherosclerosis
Abstract： To investigate the effect and mechanism of serum amyloid A (SAA) on the expression of scavenger receptor class B type Ⅰ (SR-BⅠ) and inflammatory response in THP-1 macrophages,the human THP-1 cells were treated with SAA and p38-MAPK agonist (anisomycin) or p38-MAPK inhibitor (SB203580).Then,the expressions of SR-BⅠ,phosphorylated p38-MAPK and inflammatory factors (MCP-1,TNF-α,IL-1β) were examined by real-time quantitative PCR,Western blotting and ELISA,respectively.The results showed that,compared with control group,SAA increased the levels of inflammatory factors (MCP-1,TNF-α,IL-1β),down-regulated the expressions of SR-BⅠ,and up-regulated the expression of phosphorylated p38-MAPK protein in a concentration-and time-dependent manner in THP-1 cells (P ＜ 0.05).After treatment with SAA and p38-MAPK agonist (anisomycin) in THP-1 cells,the expression of SR-BⅠ was down-regulated,and the levels of inflammatory factors and phosphorylated p38-MAPK protein expression were increased,compared with the group only treated by SAA (P ＜ 0.05).In contrast,the SR-BⅠ expression was up-regulated,whereas inflammatory factors and phosphorylated p38-MAPK protein expressions were decreased after the cells were treated with SAA and p38-MAPK inhibitor (SB203580) (P ＜ 0.05).The results suggest that SAA-promoted inflammatory response in THP-1 macrophages may be through the phosphorylation of p38-MAPK and inhibition of SR-BⅠ expression.
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