冠心平含药血清对LPS诱导的RAW264.7巨噬细胞极化的影响

周冠进; 孙玉婷; 周李煜; 陈韦凯; 掌琳惠; 胡文祺; 刘福明; 袁冬平

冠心平含药血清对LPS诱导的RAW264.7巨噬细胞极化的影响

1.
南京中医药大学附属医院/江苏省中医院，江苏南京 210029
2.
南京中医药大学药学院，江苏南京 210023

计量
- 文章访问数: 760
- HTML全文浏览量: 14
- PDF下载量: 388
- 被引次数: 0
出版历程
- 刊出日期: 2020-05-10

Effects of Guanxinping-Containing Serum on RAW 264.7 Macrophages Polarization Induced by LPS

1.
Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China
2.
School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China

摘要

摘要: 目的探讨冠心平（GXP）含药血清对LPS诱导的RAW264.7巨噬细胞极化的调控作用。方法 RAW264.7巨噬细胞分为对照组、模型组、GXP低、中、高剂量组，100 ng/mL LPS刺激12 h诱导M1型极化模型，不同浓度GXP含药血清进行干预。ELISA法检测巨噬细胞上清肿瘤坏死因子-α（TNF-α）、转化生长因子-β1（TGF-β1）含量；流式细胞术检测M1、M2型巨噬细胞特征性表面标记分子CD86、CD206表达水平；qPCR法检测巨噬细胞CD86、CD206 mRNA表达情况。结果冠心平高剂量显著减少巨噬细胞TNF-α分泌（P<0.01），各剂量减少TGF-β1分泌（P<0.01）；冠心平低、高剂量显著降低M1型巨噬细胞特征性分子CD86表达（P<0.05），显著升高M2型巨噬细胞特征性分子CD206表达（P<0.01）；同时冠心平CD206 mRNA表达显著增加（P<0.05）。结论冠心平含药血清能够抑制LPS诱导的巨噬细胞M1型极化而促进M2型极化，这或许是冠心平治疗动脉粥样硬化的潜在机制之一。
- 冠心平 /
- 动脉粥样硬化 /
- 巨噬细胞 /
- 极化
Abstract: OBJECTIVE To investigate the effects of Guanxinping (GXP) on RAW264.7 macrophage polarization induced by LPS. METHODS Macrophages were divided into control group， model group and low-， mid-， high-dose of GXP groups. Cells were starved for 24 hours before intervention with drug-containing serum of rats. The characteristic molecules of macrophage polarization in cell supernatant， including tumor necrosis factor α (TNF-α) and transforming growth factor β(TGF-β) were detected by ELISA; the expression levels of M1 and M2 macrophage surface molecules CD86 and CD206 were detected by flow cytometry; the expression of mRNA of CD86 and CD206 were detected by qPCR. RESULTS Compared to the model group， high-dose of GXP decreased the secretion of TNF-α (P<0.01); low-， mid-， high-dose of GXP decreased the secretion of TGF-β1 (P<0.01) in macrophage supernatant. Low- and high- dose of GXP decreased the expressions of CD86 (P<0.05) and increased the expression of CD206 (P<0.01). There were no significant difference in the mRNA expression of CD86 between the GXP groups and model group， but GXP increased the mRNA expression of CD206. CONCLUSION GXP can inhibit the polarization of macrophages towards M2， which may be one of the mechanisms of GXP in the treatment of atherosclerosis.
- Guanxinping /
- atherosclerosis /
- macrophages /
- polarization

HTML全文

参考文献(13)

[1]	FANG SH，XU YW，ZHANG Y，et al．Irgm1 promotes M1 but not M2 macrophage polarization in atherosclerosis pathogenesis and development[J]．Atherosclerosis，2016，251：282-290．
[2]	HANSSON GK，HERMANSSON A．The immune system in atherosclerosis[J]．Nat Immunol，2011，12(3)：204-212．
[3]	TABAS I，BORNFELDT KE．Macrophage phenotype and function in different stages of atherosclerosis[J]．Circ Res，2016，118(4)：653-667．
[4]	ROBBINS CS，CHUDNOVSKIY A，RAUCH PJ，et al．Extramedullary hematopoiesis generates Ly-6C(high) monocytes that infiltrate atherosclerotic lesions[J]．Circulation，2012，125(2)：364-374．
[5]	白瑞娜，郗瑞席，冯志博，等．巨噬细胞与动脉粥样硬化：亚型及功能[J]．中国循环杂志，2014，29(5)：393-395．
[6]	FROSTEGARD J，ULFGREN AK，NYBERG P，et al．Cytokine expression in advanced human atherosclerotic plaques：dominance of pro-inflammatory (Th1) and macrophage-stimulating cytokines[J]．Atherosclerosis，1999，145(1)：33-43．
[7]	WEBER C，NOELS H．Atherosclerosis：current pathogenesis and therapeutic options[J]．Nat Med，2011，17(11)：1410-1422．
[8]	QIAO JH，TRIPATHI J，MISHRA NK，et al．Role of macrophage colony-stimulating factor in atherosclerosis：studies of osteopetrotic mice[J]．Am J Pathol，1997，150(5)：1687-1699．
[9]	STONEMAN V，BRAGANZA D，FIGG N，et al．Monocyte/macrophage suppression in CD11b diphtheria toxin receptor transgenic mice differentially affects atherogenesis and established plaques[J]．Circ Res，2007，100(6)：884-893．
[10]	黄杰，章莹，严婧，等．铁皮石斛多糖对脂多糖诱导的巨噬细胞免疫调节作用[J]．中国药学杂志，2017，52(7)：548-552．
[11]	MOORE K，TABAS I．Macrophages in the pathogenesis of atherosclerosis[J]．Cell，2011，145(3)：341-355．
[12]	GALKINA EV，LEY K．Immune and inflammatory mechanisms of atherosclerosis[J]．Annu Rev Immunol，2009，27(1)：165-197．
[13]	ZHAO XN，LI YN，WANG YT．Interleukin-4 regulates macrophage polarization via the MAPK signaling pathway to protect against atherosclerosis[J]．Genet Mol Res，2016，15(1)：1-9.