Norisoboldine Attenuates Sepsis-Induced Acute Lung Injury by Modulating Macrophage Polarization via PKM2/HIF-1α/PGC-1α Pathway
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- Chen Qi
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
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- Shao Xuebo
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
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- He Yanyan
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
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- Lu Enkui
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
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- Zhu Lijun
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
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- Tang Weidong
- Department of Critical Care Medicine, the First People's Hospital of Fuyang District
書誌事項
- タイトル別名
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- Norisoboldine Attenuates Sepsis-Induced Acute Lung Injury by Modulating Macrophage Polarization <i>via</i> PKM2/HIF-1α/PGC-1α Pathway
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抄録
<p>This study aimed to investigate the effect of norisopoldine (NOR) on acute lung injury in septic mice. Lipopolysaccharide (LPS) was used to establish sepsis induced acute lung injury (ALI) in mice. The dry and wet weight of mice lung was detected, and the pathological changes of lung were observed by hematoxylin and eosin (H&E) staining. Bronchoalveolar lavage fluid (BALF) was detected. Inflammatory factors in BALF were detected by enzyme-linked immunosorbent assay (ELISA). The polarization of macrophages in lung tissue was detected by flow cytometry. The markers of M1 and M2 macrophages were detected by RT-PCR. LPS induced RAW264.7 cells were treated with NOR. Inflammatory response, macrophage polarization, glycolysis, and M2 pyruvate kinase (PKM2)/hypoxia inducible factor-1α (HIF-1α)/peroxisome proliferator activated receptor-γ co-activator 1-α (PGC-1α) signaling pathway were detected. NOR could effectively alleviate sepsis induced ALI, and reduce the number of total cells, total protein concentration, neutrophils, macrophages in BALF. NOR decreased the level of inflammatory factors and promoted macrophages from M1 to M2 type in vivo and vitro. Moreover, NOR could activated PKM2, and inhibited PKM2 from cytoplasm to nuclear, attenuated HIF-1α expression, and increased PGC-1α and peroxisome proliferator-activated receptor (PPAR)-γ expression. In addition, NOR inhibited glycolysis and promoted oxidative phosphorylation in RAW264.7 cells. Furthermore, PKM2 inhibitors could reverse the effect of NOR on PKM2/HIF-1α/PGC-1α signaling pathway in RAW264.7 cells. NOR alleviated sepsis induced AIL in mice, inhibited the inflammatory response, promote M2 polarization of macrophages through regulating PKM2/HIF-1α/PGC-1α signaling pathway.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 44 (10), 1536-1547, 2021-10-01
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390852514694800256
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- NII論文ID
- 130008095748
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 031713666
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- PubMed
- 34602563
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可