Anti-inflammatory effects of apoprotein A Ⅰ are mediated via modulating macrophage polarity
10.3760/cma.j.issn.0253-3758.2014.02.007
- VernacularTitle:载脂蛋白AⅠ改变炎症型巨噬细胞极性发挥抗炎作用
- Author:
Quanzhong LI
1
;
Zhenli ZHAI
;
Weihong MA
;
Zongjie QIAN
Author Information
1. 541001,桂林医学院附属医院心内科
- Keywords:
Atherosclerosis;
Apolipoprotein A-Ⅰ;
Macrophages;
Inflammation
- From:
Chinese Journal of Cardiology
2014;42(2):132-135
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the anti-inflammatory mechanisms of high density lipoprotein (HDL) by observing the effects of apoprotein (apo) A Ⅰ,a major protein component of HDL,on the inflammatory macrophage cell polarity.Methods Cultured mice marrow-derived macrophages were stimulated with lipopolysaccharide and interferon after 10 μg/ml of apoA Ⅰ were added to the macrophages for 24 hours.The expression of membrane molecules CD16/32,CD206 were detected by fluorescence activated cell sorting (FACS).ELISA was used to detect the secretion of IL-10 and IL-12.Real-time quantitative PCR was used to detect the mRNA expression of TLR4,MyD88 and IRF5.Results Compared to macrophages stimulated by interferon and lipopolysaccharide but without pretreatment with apoA Ⅰ,pre-incubation with apoA Ⅰ significantly downregulated the expression of CD16/32 (91.17％ ± 1.99％ vs.50.47％ ± 1.02％,P ＜0.05),IL-12 [(747.27 ±3.74) pg/ml vs.(73.80 ±4.56) pg/ml,P ＜0.05],upregulated the expression of CD206 (0.33％ ± 0.12％ vs.3.00％ ± 0.36％,P ＜ 0.05),IL-10 expression [(23.56 ±4.30) pg/ml vs.(32.91 ± 2.47) pg/ml,P ＜ 0.05],and reduced the mRNA expression of TLR4(1.000±0.025 vs.0.708 ±0.003,P＜0.05),MyD88(1.591 ±0.005 vs.1.341 ±0.005,P＜ 0.05),IRF5 (0.954 ± 0.005 vs.0.463 ± 0.003,P ＜ 0.05).Conclusion ApoA Ⅰ enhances the switch of inflammatory macrophages to anti-inflammatory macrophages possibly through inhibiting TLR4-MyD88-IRF5 pathway.
