Effective-compound combination inhibits the M2-like polarization of macrophages and attenuates the development of pulmonary fibrosis by increasing autophagy through mTOR signaling

自噬 巨噬细胞极化 PI3K/AKT/mTOR通路 化学 肺纤维化 博莱霉素 下调和上调 M2巨噬细胞 纤维化 细胞生物学 癌症研究 信号转导 药理学 医学 生物 内科学 细胞凋亡 体外 巨噬细胞 生物化学 基因 化疗
作者
Peng Zhao,Zehui Cai,Yange Tian,Junzi Li,Kangchen Li,Minyan Li,Yunping Bai,Jiansheng Li
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:101: 108360-108360 被引量:10
标识
DOI:10.1016/j.intimp.2021.108360
摘要

The M2 polarization of macrophages substantially contributes to the progression of pulmonary fibrosis (PF). Effective-compound combination (ECC), which is composed of isoliquiritigenin, icariin, nobiletin, peimine, and paeoniflorin, ameliorated bleomycin-induced PF in rats. Hence, we investigated the anti-PF mechanism of ECC with a focus on the suppression of M2 polarization in macrophages in vivo and in vitro.The PF rat model was generated via the intratracheal instillation of bleomycin. Histological changes, M2 macrophages, and profibrotic mediators were detected. The M2 polarization model was generated by incubating macrophages with IL-4. Quantitative PCR and Western blotting were used to measure mRNA and protein levels, respectively.ECC attenuated bleomycin-induced PF in rats, which might be associated with reduced macrophage infiltration, M2 polarization, and profibrotic mediator expression. Furthermore, ECC significantly suppressed M2 polarization in IL-4-treated macrophages, which was accompanied by the upregulation of autophagy. An autophagy inhibitor abrogated the inhibitory effect of ECC on M2 polarization. In addition, ECC decreased the levels of p-p70S6K/p-4EBP and p-AKT473/p-GSK3β, which are critical regulators of autophagy.ECC can ameliorate PF, which might be associated with the inhibition of M2 polarization through the promotion of autophagy via mTOR signaling suppression.
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