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Article Navigation >  Journal of Pharmaceutical Practice and Service  > 2019  >  37(1): 32-36,41

DI Xuemei, YUAN Yaohui, ZHANG Chao, GAO Yue. Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 32-36,41. doi: 10.3969/j.issn.1006-0111.2019.01.008
Citation: DI Xuemei, YUAN Yaohui, ZHANG Chao, GAO Yue. Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 32-36,41. doi: 10.3969/j.issn.1006-0111.2019.01.008
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Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages

doi: 10.3969/j.issn.1006-0111.2019.01.008
  • 1.

    First Maternity and Infant Hospital, Tongji University, Shanghai 201204, China

  • 2.

    School of Pharmaceutical Sciences, Shandong University of Traditional Chinese Medicine, Jinan 250355, China

  • 3.

    Experimental and Teaching Center, School of Pharmacy, Naval Medical University, Shanghai 200433, China

  • Received Date: 2018-07-06
  • Rev Recd Date: 2018-12-31
  • Objective To investigate the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages. Methods The expression of CCL18 mRNA was detected by real time PCR. The expression of CCL18 protein was assessed by Elisa. The expression of IL-4 receptor was measured by flow cytometry. The STAT6 phosphorylation was measured by Elisa. The activity of JAK kinase was detected by Z″-LYTETM kinase assay. Results AS-Ⅳ significantly down-regulated the expression of CCL18 in U937 macrophages stimulated by IL-4 with a dose-dependent manner. However, AS-Ⅳ had no significant effect on IL-4 receptor subunit expression. The STAT6 phosphorylation was inhibited by AS-Ⅳ, but the effect was less than AS1517499; the activity of JAK1, JAK3 and TYK2 kinase were inhibited by AS-Ⅳ. Conclusion AS-Ⅳ could inhibit the expression of CCL18 in U937 macrophages stimulated by IL-4. One of the suggested mechanisms was due to inhibition of JAK kinase activity, which caused STAT6 transcriptional activity down and inhibited CCL18 gene expression.
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    [2] 蒋云峰.黄芪桃红汤治疗特发性肺纤维化24例[J].吉林中医药,2003,23(11):14.
    [3] 李丽君,范盎然,葛东宇,等.黄芪当归对药对特发性肺纤维化小鼠生存状况及组织修复相关基因表达水平的影响[J].环球中医药,2015,8(12):1441-1445.
    [4] 李红,王胜,沈明霞,等.黄芪甲苷对特发性肺纤维化模型大鼠肺组织碱性成纤维细胞生长因子(bFGF)表达的影响[J].西部中医药,2015,28(12):21-24.
    [5] 李红,沈明霞,谢海彬,等.黄芪甲苷对特发性肺纤维化模型大鼠肺组织CD34表达的影响[J].西部中医药,2015,28(9):6-10.
    [6] PRASSE A,PECHKOVSKY D V,TOEWS G B,et al. CCL18 as an indicator of pulmonary fibrotic activity in idiopathic interstitial pneumonias and systemic sclerosis[J]. Arthriti Rheumat,2007,56(5):1685-1693.
    [7] CAI M,BONELLA F,HE X,et al. CCL18 in serum,BAL fluid and alveolar macrophage culture supernatant in interstitial lung diseases[J]. Respir Med,2013,107(9):1444-1452.
    [8] PRASSE A,PROBST C,BARGAGLI E,et al. Serum CC-chemokine ligand 18 concentration predicts outcome in idiopathic pulmonary fibrosis[J]. Am J Respir Crit Care Me,2009,179(8):717-723.
    [9] HIESHIMA K,IMAI T,BABA M,et al. A novel human CC chemokine PARC that is most homologous to macrophage-inflammatory protein-1 alpha/LD78 alpha and chemotactic for T lymphocytes,but not for monocytes[J]. J Immunol,1997,159(3):1140-1149.
    [10] Kodelja V,Müller C,Politz O,et al. Alternative macrophage activation-associated CC-chemokine-1,a novel structural homologue of macrophage inflammatory protein-1 alpha with a Th2-associated expression pattern.[J]. J Immunol,1998,160(3):1411-1418.
    [11] PRASSE A,PECHKOVSKY D V,TOEWS G B,et al. A vicious circle of alveolar macrophages and fibroblasts perpetuates pulmonary fibrosis via CCL18[J]. Am J Respi Crit Care Med,2006,173(7):781-792.
    [12] PECHKOVSKY D V,PRASSE A,KOLLERT F,et al. Alternatively activated alveolar macrophages in pulmonary fibrosis-mediator production and intracellular signal transduction[J]. Clin Immunol,2010,137(1):89-101.
    [13] ANDO M,MIYAZAKI E,FUKAMI T,et al. Interleukin-4-producing cells in idiopathic pulmonary fibrosis:an immunohistochemical study[J]. Respirology,1999,4(4):383-391.
    [14] WALLACE W A,HOWIE S E. Immunoreactive interleukin 4 and interferon gamma expression by type Ⅱ alveolar epithelial cells in interstitial lung disease[J].J Pathol,1999,187(4):475-480.
    [15] SCHUTYSER E,RICHMOND A,DAMME J V. Involvement of CC chemokine ligand 18(CCL18) in normal and pathological processes[J]. J Leuk Biol,2005,78(1):14-26.
    [16] ATAMAS S P,LUZINA I G,CHOI J,et al. Pulmonary and activation-regulated chemokine stimulates collagen production in lung fibroblasts[J]. Am J Respir Cell Mol Biol,2003,29(6):743-749.
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Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages

doi: 10.3969/j.issn.1006-0111.2019.01.008
  • 1. First Maternity and Infant Hospital, Tongji University, Shanghai 201204, China
  • 2. School of Pharmaceutical Sciences, Shandong University of Traditional Chinese Medicine, Jinan 250355, China
  • 3. Experimental and Teaching Center, School of Pharmacy, Naval Medical University, Shanghai 200433, China
  • Received Date: 2018-07-06
  • Rev Recd Date: 2018-12-31

Abstract: Objective To investigate the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages. Methods The expression of CCL18 mRNA was detected by real time PCR. The expression of CCL18 protein was assessed by Elisa. The expression of IL-4 receptor was measured by flow cytometry. The STAT6 phosphorylation was measured by Elisa. The activity of JAK kinase was detected by Z″-LYTETM kinase assay. Results AS-Ⅳ significantly down-regulated the expression of CCL18 in U937 macrophages stimulated by IL-4 with a dose-dependent manner. However, AS-Ⅳ had no significant effect on IL-4 receptor subunit expression. The STAT6 phosphorylation was inhibited by AS-Ⅳ, but the effect was less than AS1517499; the activity of JAK1, JAK3 and TYK2 kinase were inhibited by AS-Ⅳ. Conclusion AS-Ⅳ could inhibit the expression of CCL18 in U937 macrophages stimulated by IL-4. One of the suggested mechanisms was due to inhibition of JAK kinase activity, which caused STAT6 transcriptional activity down and inhibited CCL18 gene expression.

DI Xuemei, YUAN Yaohui, ZHANG Chao, GAO Yue. Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 32-36,41. doi: 10.3969/j.issn.1006-0111.2019.01.008
Citation: DI Xuemei, YUAN Yaohui, ZHANG Chao, GAO Yue. Research on the effect and mechanism of astragalus Ⅳ(AS-Ⅳ) on the expression of CCL18 in U937 macrophages[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 32-36,41. doi: 10.3969/j.issn.1006-0111.2019.01.008
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