Luteolin Alters Macrophage Polarization to Inhibit Inflammation

炎症 M2巨噬细胞 木犀草素 CD86 川地163 下调和上调 促炎细胞因子 巨噬细胞极化 巨噬细胞 肿瘤坏死因子α 脂多糖 化学 白细胞介素 流式细胞术 免疫学 细胞生物学 细胞因子 生物 T细胞 免疫系统 生物化学 体外 类黄酮 基因 抗氧化剂
作者
Shuxia Wang,Meng Cao,Shuhang Xu,Jianfeng Shi,Xiaodong Mao,Xiaoming Yao,Chao Liu
出处
期刊:Inflammation [Springer Nature]
卷期号:43 (1): 95-108 被引量:131
标识
DOI:10.1007/s10753-019-01099-7
摘要

Luteolin is a natural flavonoid compound derived from vegetables, fruits, and herbs with potent anti-inflammatory activity. Macrophage polarization is important in the development and progression of inflammation. However, whether luteolin can inhibit inflammation by regulating the polarized phenotypes of macrophages remains unknown. The aim of this study was to investigate the effects of luteolin on the inflammatory polarization of macrophages and the underlying mechanisms. RAW264.7 macrophages were induced to M1 polarization by stimulation with lipopolysaccharide plus interferon-γ or to M2 polarization with interleukin 4 (IL-4), simultaneously, accompanied with different concentrations of luteolin. Laser confocal microscopy was used to observe cell morphology; flow cytometry was employed to detect the expression of membrane surface molecule CD86 and CD206; qPCR was performed to examine the mRNA expression of M1 markers (iNOS, IL-1β, IL-6) and M2 markers (Arg1, CD206, CD163, IL-10, and IL-13), respectively; ELISA was used to examine the levels of IL-6, TNF-α, and IL-10; and Western blotting was used to evaluate the p-STAT3 and p-STAT6 protein pathway. The morphology of activated M1 macrophages changed significantly, developing dendritic characteristics. After luteolin treatment, the expression of M1-type proinflammatory mediators and the surface marker CD86 were decreased evidently, but those of M2-related anti-inflammatory factors and CD206 were increased markedly. Moreover, p-STAT3 was downregulated and p-STAT6 was upregulated in a dose-dependent manner. Conclusion, luteolin can alter the M1/M2 polarization of macrophages, thereby playing an anti-inflammatory role via downregulation of p-STAT3 and upregulation of p-STAT6. Therefore, luteolin may be potentially valuable to inhibit inflammation.
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