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Induction of autophagy via the TLR4/NF-κB signaling pathway by astragaloside Ⅳ contributes to the amelioration of inflammation in RAW264.7 cells.

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机构: [a]Yunnan Provincial Key Laboratory of Molecular Biology for Sinomedicine, Yunnan University of Chinese Medicine, Kunming, Yunnan, China [b]The First Clinical Medicine College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China [c]Central Laboratory, Kunming Medical University Second Hospital, Kunming, Yunnan, China [d]The Key Laboratory of Molecular Epigenetics of MOE, Institute of Genetics and Cytology, Northeast Normal University, Changchun, Jilin, China [e]PingHu Hospital Shenzhen University, Shenzhen University, Shenzhen, Guangdong, China [f]Key Laboratory of Microcosmic Syndrome Differentiation, Education Department of Yunnan, Kunming, Yunnan University of Chinese Medicine, Yunnan, China
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关键词: Inflammation Autophagy TLR4/NF-κB signaling pathway Astragaloside Ⅳ

摘要:
Cigarette smoking-related lung injury is one of the most common and fatal etiologies of many respiratory diseases, for which no effective interventions are available. Astragaloside Ⅳ (ASⅣ) is an active component extracted from Astragalus membranaceus. It is prescribed as a treatment for upper respiratory tract infections. Here, we report the potential anti-inflammatory effects and mechanisms of ASⅣ on cigarette smoking extract- (CSE)-exposed RAW264.7 cells. Murine macrophages were exposed to CSE, followed by administration of ASⅣ at 25-100 μg/mL for 24 h. ASⅣ significantly rescued CSE-induced cell death by inhibition of release pro-inflammatory cytokines. We measured autophagy as an intracellular scavenger by analyzing autophagic flux using tandem mRFP-GFP-LC3 fluorescence microscopy. Following administration with ASⅣ in CSE-exposed RAW264.7 cells, there was a notable increase in autophagosomes and a range of autophagic vacuoles were generated, as seen with transmission electron microscopy. Loss of autophagy following transfection siRNA aggravated inflammatory injury and release of inflammatory cytokines. Mechanistically, ASⅣ-triggered autophagy is mediated by the TLR4/NF-κB signaling pathway to reduce inflammation. Taken together, our findings suggest that ASⅣ acts stimulates autophagy, and that ASⅣ induces autophagy by inhibiting the TLR4/NF-κB signaling pathway, contributing to alleviation of inflammation. Copyright © 2021 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.

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出版当年[2020]版:
大类 | 2 区 医学
小类 | 2 区 药学 3 区 医学:研究与实验
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 医学:研究与实验 2 区 药学
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第一作者机构: [a]Yunnan Provincial Key Laboratory of Molecular Biology for Sinomedicine, Yunnan University of Chinese Medicine, Kunming, Yunnan, China
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通讯机构: [a]Yunnan Provincial Key Laboratory of Molecular Biology for Sinomedicine, Yunnan University of Chinese Medicine, Kunming, Yunnan, China [b]The First Clinical Medicine College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China [f]Key Laboratory of Microcosmic Syndrome Differentiation, Education Department of Yunnan, Kunming, Yunnan University of Chinese Medicine, Yunnan, China
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