Astragaloside IV Alleviates the Experimental DSS-Induced Colitis by Remodeling Macrophage Polarization Through STAT Signaling
Autor: | Jian Zhang, Yan Lin, Jian-Qin Kang, Ya-Long Zhang, Shibo Guo, Jun-Long Zhao, Lianlian Tian, Nini Zhang, Xun Jiang, Lei Shang |
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Rok vydání: | 2021 |
Předmět: |
Immunology
Anti-Inflammatory Agents Macrophage polarization Inflammatory bowel disease pro-resolving macrophage Mice macrophages polarization inflammatory bowel disease In vivo Animals Humans Immunology and Allergy Medicine Macrophage Medicine Chinese Traditional Colitis Original Research business.industry Macrophages Dextran Sulfate Cell Differentiation Astragalus propinquus Saponins RC581-607 Inflammatory Bowel Diseases medicine.disease Phenotype Triterpenes In vitro Mice Inbred C57BL Disease Models Animal STAT Transcription Factors astragaloside IV (AS-IV) STAT signaling Cancer research Cytokines Immunologic diseases. Allergy business Function (biology) Signal Transduction |
Zdroj: | Frontiers in Immunology, Vol 12 (2021) Frontiers in Immunology |
ISSN: | 1664-3224 |
Popis: | 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. |
Databáze: | OpenAIRE |
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