Research on the effect and mechanism of astragalus Ⅳ (AS-Ⅳ) on the expression of CCL18 in U937 macrophages
10.3969/j.jssn.1006-0111.2019.01.008
- VernacularTitle:黄芪甲苷抑制U937巨噬细胞CCL18表达及其作用机制研究
- Author:
Xuemei DI
1
;
Yaohui YUAN
;
Chao ZHANG
;
Yue GAO
Author Information
1. 同济大学附属第一妇婴保健院
- Keywords:
astragalus Ⅳ;
macrophages;
CCL18;
idiopathic pulmonary fibrosis
- From:
Journal of Pharmaceutical Practice
2019;37(1):32-36,41
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of astragalusⅣ (AS-Ⅳ) on the expression of CCL18in U937macrophages.Methods The expression of CCL18mRNA was detected by real time PCR.The expression of CCL18protein was assessed by Elisa.The expression of IL-4receptor was measured by flow cytometry.The STAT 6phosphorylation was measured by Elisa.The activity of JAK kinase was detected by Z″-LYTETMkinase assay.Results AS-Ⅳsignificantly down-regulated the expression of CCL18in U937macrophages stimulated by IL-4with a dose-dependent manner.However, AS-Ⅳhad no significant effect on IL-4receptor subunit expression.The STAT6phosphorylation was inhibited by AS-Ⅳ, but the effect was less than AS1517499;the activity of JAK1, JAK3and TYK2kinase were inhibited by AS-Ⅳ.Conclusion AS-Ⅳcould inhibit the expression of CCL18in U937macrophages stimulated by IL-4.One of the suggested mechanisms was due to inhibition of JAK kinase activity, which caused STAT6transcriptional activity down and inhibited CCL18gene expression.
