Yin Xuehong, Pang Chunyan, Bai Li, Zhang Ying, Geng Lixia
First Affiliated Hospital, Baotou Medical College, Baotou 014040, China.
First Affiliated Hospital, Baotou Medical College, Baotou 014040, China. *Corresponding author, E-mail:
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Mar;32(3):332-8.
To investigate the effects of adipose-derived stem cells (ADSCs) on M1/M2 macrophages and whether ADSCs are able to promote the polarization from M1 macrophages to M2 macrophages.
M1 macrophages were induced from J774.1 macrophages by 24-hour stimulation of lipopolysaccharide (LPS) and interferon γ (IFN-γ), and M2 macrophages were induced from J774.1 macrophages by interleukin 4 (IL-4) for another 24 hours. Then M1/M2 macrophages were separately cultured in the presence of ADSCs for 24 hours. The M1/M2 macrophages and their corresponding supernatants were collected for further analysis. The expressions of IL-6, tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS), CC chemokine ligand 2 (CCL2), CD86, arginase 1 (Arg1), mannose receptors/CD206 (MR/CD206), IL-10, found in inflammatory zone 1 (FIZZ1), chitinase 3-like 3 (Ym-1) were detected by real-time PCR and ELISA.
ADSCs significantly decreased the levels of IL-6, TNF-α, iNOS, CCL2 and CD86, and increased the levels of Arg1, CD206 and IL-10 in M1 macrophages. In the supernatant of M1 macrophages, the expressions of IL-6 and TNF-α were reduced, while those of CD206 were enhanced. In M2 macrophages, ADSCs resulted in down-regulation of IL-6, TNF-α, iNOS, CD86 and up-regulation of Arg1, CD206, FIZZ-1, Ym-1 and IL-10. In the supernatant of M2 macrophages, the expression levels of IL-6 and TNF-α were down-regulated and those of CD206 were up-regulated.
ADSCs can inhibit the gene expression of M1 macrophages and promote the gene expression of M2 macrophages, as well as mediate the polarization from M1 macrophages to M2 macrophages.
研究脂肪来源干细胞（ADSCs）对M1/M2巨噬细胞的影响，以及ADSCs是否能够促进M1巨噬细胞向M2巨噬细胞极化。
通过脂多糖（LPS）和干扰素γ（IFN-γ）刺激24小时从J774.1巨噬细胞诱导出M1巨噬细胞，通过白细胞介素4（IL-4）再刺激24小时从J774.1巨噬细胞诱导出M2巨噬细胞。然后将M1/M2巨噬细胞分别与ADSCs共同培养24小时。收集M1/M2巨噬细胞及其相应的上清液用于进一步分析。通过实时PCR和ELISA检测炎症区1（FIZZ1）、几丁质酶3样3（Ym-1）中白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、诱导型一氧化氮合酶（iNOS）、CC趋化因子配体2（CCL2）、CD86、精氨酸酶1（Arg1）、甘露糖受体/CD206（MR/CD206）、IL-10的表达。
ADSCs显著降低M1巨噬细胞中IL-6、TNF-α、iNOS、CCL2和CD86的水平，并增加Arg1、CD206和IL-10的水平。在M1巨噬细胞的上清液中，IL-6和TNF-α的表达降低，而CD206的表达增强。在M2巨噬细胞中，ADSCs导致IL-6、TNF-α、iNOS、CD86下调，Arg1、CD206、FIZZ-1、Ym-1和IL-10上调。在M2巨噬细胞的上清液中，IL-6和TNF-α的表达水平下调，CD206的表达上调。
ADSCs可抑制M1巨噬细胞的基因表达，促进M2巨噬细胞的基因表达，并介导M1巨噬细胞向M2巨噬细胞极化。
