巨噬细胞极化
脂多糖
M2巨噬细胞
TLR4型
细胞生物学
细胞因子
巨噬细胞
化学
肿瘤坏死因子α
炎症
流式细胞术
促炎细胞因子
一氧化氮
分子生物学
生物
一氧化氮合酶
MAPK/ERK通路
NF-κB
信号转导
免疫学
p38丝裂原活化蛋白激酶
体外
生物化学
作者
Shan Gao,Yili Wang,Dan Li,Yuying Guo,Meifeng Zhu,Shixin Xu,Jingyuan Mao,Guanwei Fan
出处
期刊:Inflammation
[Springer Nature]
日期:2018-09-14
卷期号:42 (1): 264-275
被引量:23
标识
DOI:10.1007/s10753-018-0891-7
摘要
TanshinoneIIA (TanIIA) has been demonstrated to possess numerous biological effects. However, the specific effect of TanIIA on macrophage polarization has not been reported. In this study, it was revealed that TanIIA might play a pivotal role in macrophage polarization. As our results indicated, cell morphology was changed in RAW264.7 cells which were treated with LPS or LPS/TanIIA (0.1 μM, 1 μM, 10 μM). Subsequently, pro-inflammatory cytokine TNF-α and anti-inflammatory cytokine IL-10 were measured by ELISA kits. Furthermore, TanIIA enhanced the expression of M2 macrophage markers (Arg1 and FIZZ1) and decreased the expression of markers associated with M1 macrophage polarization (iNOS and IL-1β). Increased expression of CD206 was also detected by flow cytometry in TanIIA-treated groups. Mechanistically, it was revealed that TanIIA modulated macrophage polarization by ameliorating mitochondrial function and regulating TLR4-HMGB1/CEBP-β pathway. In addition, increased expression of miR-155 was observed in RAW264.7 cells incubated with LPS and were effectively inhibited by TanIIA. Taken together, it was suggested that TanIIA inhibits inflammatory response and promotes macrophage polarization toward an M2 phenotype, which provides new evidence for the anti-inflammation activity of TanIIA.
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