ArticleJournal of molecular histology2025
Echinacoside ameliorates bleomycin-induced idiopathic pulmonary fibrosis by regulating macrophage polarization.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Echinacoside Improves Pulmonary Vascular Remodeling by Regulating the L- and T-Type CaPulmonary circulation · 2026Article
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is identified as a chronic, progressive fibrotic interstitial pneumonia of unknown cause. Echinacoside (ECH) is a phenylethanoid glycoside extracted from Cistanche deserticola, which exhibits noteworthy anti-oxidant and anti-inflammatory activities and can protect against renal, myocardial, and kidney fibrosis. This study aimed to assess the therapeutic effect of ECH on IPF by using cellular and animal experiments. Bleomycin (BLM)-induced IPF mice and transforming growth factor (TGF)-β1-treated human embryonic lung fibroblasts (MRC-5) were respectively used as animal and cellular models of IPF, which were then subjected to ECH treatment. Mouse pulmonary tissues were harvested for hematoxylin and eosin (H&E), Masson's trichrome, immunohistochemical, and immunofluorescence staining, RT-qPCR, and western blotting to determine pulmonary histological changes and the expression of fibrosis-related genes (α-SMA, fibronectin, and COL1A1), M2 macrophage markers (CD206, CD163, Arg-1, and YM-1), and phosphorylated JAK2 and STAT3. Bronchoalveolar lavage fluid (BALF) was collected to detect total protein contents, total inflammatory cell counts, pro-inflammatory cytokine (TNF-α and IL-1β) levels, and pro-fibrosis factor TGF-β content. Cell viability and migration and ⍺-SMA, fibronectin, COL1A1, and phosphorylated JAK2 and STAT3 levels in MRC-5 cells were assessed through CCK-8 assay, wound healing assay, RT-qPCR, and western blotting. ECH administration significantly mitigated BLM-induced pulmonary inflammation and fibrosis in mice. ECH decreased total protein contents, total leukocyte counts, TNF-α and IL-1β levels, and TGF-β contents in BALF as well as hydroxyproline contents and α-SMA, fibronectin, COL1A1, CD206, CD163, Arg-1, and YM-1 levels in pulmonary tissues of BLM-induced IPF mice. In vitro data revealed that ECH markedly inhibited the upregulation of ⍺-SMA, fibronectin, and COL1A1 expression and cell migration induced by TGF-β1 in MRC-5 cells. From a mechanistic standpoint, ECH treatment inhibited phosphorylated JAK2 and STAT3 levels both in vivo and in vitro. ECH exhibits an anti-fibrotic effect in IPF by inhibiting pro-fibrotic M2 macrophage polarization, which might be attributed to its downregulation of the JAK2/STAT3 pathway. This discovery emphasizes the potential of ECH as a promising therapeutic agent for IPF treatment.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.