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血清淀粉样蛋白A经p38-MAPK/SR-BI途径促进巨噬细胞炎症反应

朱明燕, 王燕, 王毓, 彭凤玲, 欧含笑, 郑翔, 石金凤, 曾高峰, 莫中成^*

1南华大学医学院组织学与胚胎学教研室，衡阳 421001；南华大学附属第二医院2心血管内科；3麻醉科；4检验科，衡阳 421001

摘要

为探讨血清淀粉样蛋白A (serum amyloid A, SAA)对巨噬细胞B类I型清道夫受体(scavenger receptor class B type I, SR-BI)的表达以及炎症反应的影响及分子机制，采用SAA、p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase, p38-MAPK)激动剂anisomycin或抑制剂SB203580处理THP-1巨噬细胞，以实时定量PCR、Western blot和ELISA分别检测细胞中SR-BI、炎症因子及磷酸化p38-MAPK的表达。结果显示，与对照组相比，SAA处理THP-1细胞后，SR-BI的表达下调，而炎症因子与磷酸化p38蛋白的表达则上调，且这种效应呈浓度和时间依赖性(P < 0.05)。与SAA单独处理组比较，SAA与p38-MAPK激动剂anisomycin共孵育细胞后，细胞SR-BI表达下调，炎症因子及磷酸化p38蛋白表达增加(P < 0.05)；而SAA与p38-MAPK抑制剂SB203580 共同处理细胞后，细胞SR-BI表达增加，炎症因子及磷酸化p38蛋白表达减少(P < 0.05)。结果提示，
SAA可促进THP-1巨噬细胞炎症反应，其机制与p38-MAPK的磷酸化及SR-BI表达的下调有关。

关键词： 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

Serum amyloid A promotes the inflammatory response via p38-MAPK/SR-BI pathway in THP-1 macrophages

ZHU Ming-Yan, , WANG Yan, WANG Yu, PENG Feng-Ling, OU Han-Xiao, ZHENG Xiang, SHI Jin-Feng, ZENG Gao-Feng, MO Zhong-Cheng^*

1Department of Histology and Embryology, University of South China, Hengyang 421001, China； 2Department of Cardiovascular Medicine； 3Department of Anesthesiology and 4Department of Clinical Laboratory, the Second Affiliated Hospital of University of South China, Hengyang 421001, China

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.

Key words: scavenger receptor class B type I; serum amyloid protein A; p38-MAPK; atherosclerosis

收稿日期：2016-01-02　　录用日期：2016-03-11

通讯作者：莫中成　　E-mail: zhchmo@hotmail.com

引用本文：

朱明燕, 王燕, 王毓, 彭凤玲, 欧含笑, 郑翔, 石金凤, 曾高峰, 莫中成. 血清淀粉样蛋白A经p38-MAPK/SR-BI途径促进巨噬细胞炎症反应[J]. 生理学报 2016; 68 (3): 293-300.

ZHU Ming-Yan, , WANG Yan, WANG Yu, PENG Feng-Ling, OU Han-Xiao, ZHENG Xiang, SHI Jin-Feng, ZENG Gao-Feng, MO Zhong-Cheng. Serum amyloid A promotes the inflammatory response via p38-MAPK/SR-BI pathway in THP-1 macrophages. Acta Physiol Sin 2016; 68 (3): 293-300 (in Chinese with English abstract).