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原花青素 B2 通过激活 PPARγ 诱导小鼠巨噬细胞 M2 极化。

Procyanidin B2 Activates PPARγ to Induce M2 Polarization in Mouse Macrophages.

机构信息

Cardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University, Xi'an, China.

The Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, China.

出版信息

Front Immunol. 2019 Aug 7;10:1895. doi: 10.3389/fimmu.2019.01895. eCollection 2019.

DOI:10.3389/fimmu.2019.01895
PMID:31440258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6693435/
Abstract

Procyanidins, a subclass of flavonoids found in commonly consumed foods, possess potential anti-inflammatory activity. Manipulation of M1/M2 macrophage homeostasis is an effective strategy for the treatment of metabolic inflammatory diseases. The objective of this study was to determine the effect of procyanidins on macrophage polarization. Procyanidin B2 (PCB2), the most widely distributed natural procyanidins, enhanced the expressions of M2 macrophage markers (Arg1, Ym1, and Fizz1). PCB2 activated peroxisome proliferator-activated receptor γ (PPARγ) activity and increased the expressions of PPARγ target genes (CD36 and ABCG1) in macrophages. Inhibition of PPARγ using siRNA or antagonist GW9662 attenuated the PCB2-induced expressions of M2 macrophage markers. In addition, we identified cognate PPAR-responsive elements (PPREs) within the 5'-flanking regions of the mouse Arg1, Ym1, and Fizz1 genes. Furthermore, macrophages isolated from db/db diabetic mice showed lower expressions of M2 markers. PCB2 effectively restored the Arg1, Ym1, and Fizz1 expressions in a PPARγ-dependent manner. These findings support the notion that PCB2 regulated macrophage M2 polarization the activation of PPARγ. Our results provide a new mechanism by which procyanidins exert their beneficial anti-inflammatory effects.

摘要

原花青素是广泛存在于常见食物中的类黄酮的一个子类，具有潜在的抗炎活性。调节 M1/M2 巨噬细胞的平衡是治疗代谢性炎症性疾病的有效策略。本研究旨在确定原花青素对巨噬细胞极化的影响。原花青素 B2（PCB2）是最广泛分布的天然原花青素，增强了 M2 巨噬细胞标志物（Arg1、Ym1 和 Fizz1）的表达。PCB2 激活过氧化物酶体增殖物激活受体 γ（PPARγ）的活性，并增加巨噬细胞中 PPARγ 靶基因（CD36 和 ABCG1）的表达。使用 siRNA 或拮抗剂 GW9662 抑制 PPARγ，减弱了 PCB2 诱导的 M2 巨噬细胞标志物的表达。此外，我们在小鼠 Arg1、Ym1 和 Fizz1 基因的 5'侧翼区域内鉴定出同源的 PPAR 反应元件（PPREs）。此外，从 db/db 糖尿病小鼠中分离出的巨噬细胞表现出较低的 M2 标志物表达。PCB2 以依赖 PPARγ的方式有效地恢复 Arg1、Ym1 和 Fizz1 的表达。这些发现支持了 PCB2 通过激活 PPARγ来调节巨噬细胞 M2 极化的观点。我们的研究结果提供了一个新的机制，说明原花青素发挥其有益的抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/3d183bc0622e/fimmu-10-01895-g0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/3d183bc0622e/fimmu-10-01895-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/ec1a1989fec4/fimmu-10-01895-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/eebb553963d9/fimmu-10-01895-g0002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/33fd6021cdfb/fimmu-10-01895-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/f5451fb81daa/fimmu-10-01895-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/dc77d848f43c/fimmu-10-01895-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2d6/6693435/3d183bc0622e/fimmu-10-01895-g0007.jpg

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