ArticleImmunity, inflammation and disease2024
Dehydroandrographolide facilitates M2 macrophage polarization by downregulating DUSP3 to inhibit sepsis-associated acute kidney injury.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Adipose-derived mesenchymal stem cell-derived extracellular vesicles reduce glycolysis and polarize macrophages toward M2 phenotype in sepsis-associated acute kidney injury via the miR-574-5p/GLUT1 axis.Clinical and experimental medicine · 2026Article
- Dehydroandrographolide attenuates Toll-like receptor signaling by dual inhibition of MyD88- and TRIF-dependent pathways.Scientific reports · 2026Article
- Identification and validation of key biomarkers for chemoresistance in oral squamous cell carcinoma.BMC cancer · 2025Article
- Growth differentiation factor 11 attenuates sepsis-associated acute kidney injury by reducing inflammation and coagulation via PGC-1α/Nrf2 activation.Cellular & molecular biology letters · 2025Article
- Piezo1 activation protects against sepsis-induced myocardial dysfunction in a pilot study.Scientific reports · 2025Article
- Inflammation preservation strategy: reconciling pain control and disc resorption in lumbar disc herniation.Frontiers in immunology · 2025Review
- HBP21 Alleviates Sepsis-Induced Acute Kidney Injury by Targeting PI3K/AKT-Mediated M1 Macrophage Polarization.Mediators of inflammation · 2025Article
- Pharmacological Effects and Pharmacokinetic Profiles of Dehydroandrographolide.Mediators of inflammation · 2025Review
- Dehydroandrographolide facilitates M2 macrophage polarization by downregulating DUSP3 to inhibit sepsis-associated acute kidney injury.Immunity, inflammation and disease · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundSepsis is perceived as lethal tissue damage and significantly increases mortality in combination with acute kidney injury (AKI). M2 macrophages play important roles in the secretion of anti-inflammatory and tissue repair mediators. We aimed to study the role of Dehydroandrographolide (Deh) in sepsis-associated AKI in vitro and in vivo through lipopolysaccharide (LPS)-induced macrophages model and cecal ligation and puncture-induced AKI mice model, and to reveal the mechanism related to M2 macrophage polarization.
methodsEnzyme-linked immunosorbent assay kits were used to assess the levels of inflammatory factors. Expression of markers related to M1 macrophages and M2 macrophages were analyzed. Additionally, dual specificity phosphatase 3 (DUSP3) expression was tested. Cell apoptosis was evaluated by flow cytometry analysis and terminal-deoxynucleotidyl transferase-mediated nick end labeling staining. Moreover, renal histological assessment was performed by using hematoxylin and eosin staining.
resultsDeh reduced inflammation of THP-1-derived macrophages exposed to LPS. Besides, Deh induced the polarization of M1 macrophages to M2 and downregulated DUSP3 expression in THP-1-derived macrophages under LPS conditions. Further, DUSP3 overexpression reversed the impacts of Deh on the inflammation and M2 macrophages polarization of THP-1-derived macrophages stimulated by LPS. Additionally, human proximal tubular epithelial cells (HK-2) in the condition medium from DUSP3-overexpressed THP-1-derived macrophages treated with LPS and Deh displayed decreased viability and increased apoptosis and inflammation. The in vivo results suggested that Deh improved the renal function, ameliorated pathological injury, induced the polarization of M1 macrophages to M2, suppressed inflammation and apoptosis, and downregulated DUSP3 expression in sepsis-induced mice.
conclusionDeh facilitated M2 macrophage polarization by downregulating DUSP3 to inhibit septic AKI.
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