Astragaloside IV Alleviates the Experimental DSS-Induced Colitis by Remodeling Macrophage Polarization Through STAT Signaling.
Astragaloside IV Alleviates the Experimental DSS-Induced Colitis by Remodeling Macrophage Polarization Through STAT Signaling.
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黄芪甲苷 IV 通过 STAT 信号传导重塑巨噬细胞极化,减轻实验性 DSS 诱发的结肠炎。
DOI:
10.3389/fimmu.2021.740565
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发表时间:
2021
影响因子:
7.3
通讯作者:
Lin Y
中科院分区:
文献类型:
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作者:
Tian L;Zhao JL;Kang JQ;Guo SB;Zhang N;Shang L;Zhang YL;Zhang J;Jiang X;Lin Y
Inflammatory bowel disease (IBD) is characterized by chronic and relapsing intestinal inflammation, which currently lacks safe and effective medicine. Some previous studies indicated that Astragaloside IV (AS-IV), a natural saponin extracted from the traditional Chinese medicine herb Ligusticum chuanxiong, alleviates the experimental colitis symptoms in vitro and in vivo. However, the mechanism of AS-IV on IBD remains unclear. Accumulating evidence suggests that M2-polarized intestinal macrophages play a pivotal role in IBD progression. Here, we found that AS-IV attenuated clinical activity of DSS-induced colitis that mimics human IBD and resulted in the phenotypic transition of macrophages from immature pro-inflammatory macrophages to mature pro-resolving macrophages. In vitro, the phenotype changes of macrophages were observed by qRT-PCR after bone marrow-derived macrophages (BMDMs) were induced to M1/M2 and incubated with AS-IV, respectively. In addition, AS-IV was effective in inhibiting pro-inflammatory macrophages and promoting the pro-resolving macrophages to ameliorate experimental colitis via the regulation of the STAT signaling pathway. Hence, we propose that AS-IV can ameliorate experimental colitis partially by modulating macrophage phenotype by remodeling the STAT signaling, which seems to have an essential function in the ability of AS-IV to alleviate the pathological progress of IBD.
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影响因子:
5.5
作者:
Han X;Ding S;Jiang H;Liu G
通讯作者:
Liu G
影响因子:
5.6
作者:
Jiang, Chaolai;Zhou, Zubin;Yu, Xiaowei
通讯作者:
Yu, Xiaowei
影响因子:
7.3
作者:
Gordon S;Plüddemann A
通讯作者:
Plüddemann A
DOI:
10.4049/jimmunol.1601520
发表时间:
2017-02-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Elliott MR;Koster KM;Murphy PS
通讯作者:
Murphy PS
影响因子:
30.5
作者:
通讯作者:
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