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黄芩苷通过上调 MERTK 受体促进 M2 极化的吞噬作用。

M2 Polarization by Baicalin Enhances Efferocytosis via Upregulation of MERTK Receptor.

机构信息

* Department of Biological Science and Technology, National Pingtung University of Science and Technology, 1, Shuefu Rd., Neipu, Pingtung 91201, Taiwan.

† Flow Cytometry Center, Precision Instruments Center, National Pingtung University of Science and Technology, 1, Shuefu Rd., Neipu, Pingtung 91201, Taiwan.

出版信息

Am J Chin Med. 2018;46(8):1899-1914. doi: 10.1142/S0192415X18500957. Epub 2018 Dec 6.

Abstract

Baicalin is the main active ingredient primary isolated from the Chinese herb, Scutellaria baicalensis Georgi. Although baicalin can induce M2 macrophage polarization, we still do not know the subtype of macrophages polarized by baicalin. In this study, we characterized that murine bone marrow derived macrophages induced by M-CSF can be further polarized into M2 phenotype by baicalin. The signatures of M2 macrophages for mRNA expression like interferon regulatory factor 4 (IRF4), interleukin-10 (IL-10), MERTK and PTX3 were up-regulated. Moreover, we observed the concomitantly decreasing of tumor necrosis factor alpha (TNF- ), interferon regulatory factor 5 (IRF5), IL-6. In contrast, M2 macrophages polarized by IL-4 increased gene transcript of arginase-1 (Arg-1) and surface marker of CD206 indicates that their identity as M2 rather than M2 subtypes. Interestingly, the phagocytosis as well as efferocytosis activity were significantly enhanced in M2 macrophage polarized by baicalin and these capacities were associated with the expression of MERTK receptor. Finally, we conclude that baicalin induced M2 macrophages polarization with both elevations of efferocytosis and anti-inflammatory activity.

摘要

黄芩苷是从中国草药黄芩中分离得到的主要活性成分。尽管黄芩苷可以诱导 M2 巨噬细胞极化,但我们仍然不知道黄芩苷极化的巨噬细胞亚型。在这项研究中,我们证实了由 M-CSF 诱导的鼠骨髓来源的巨噬细胞可以被黄芩苷进一步极化成为 M2 表型。M2 巨噬细胞的 mRNA 表达特征,如干扰素调节因子 4(IRF4)、白细胞介素 10(IL-10)、MERTK 和 PTX3 上调。此外,我们观察到肿瘤坏死因子-α(TNF-α)、干扰素调节因子 5(IRF5)和白细胞介素 6(IL-6)的同时减少。相比之下,由 IL-4 极化的 M2 巨噬细胞增加了精氨酸酶 1(Arg-1)的基因转录和 CD206 表面标志物,表明它们是 M2 而不是 M2 亚型的特征。有趣的是,黄芩苷诱导的 M2 巨噬细胞的吞噬作用和胞葬作用活性显著增强,这些能力与 MERTK 受体的表达有关。最后,我们得出结论,黄芩苷诱导的 M2 巨噬细胞极化具有吞噬作用和抗炎活性的双重提高。

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