ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Investigation into the protective effects of protocatechuic acid in bleomycin-induced pulmonary remodeling and fibrosis in rats: role of MMP-2/TIMP-1 and CTGF/NOX4 pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is an irreversible and progressive interstitial lung disease that results from excessive tissue repair. Production of excessive extracellular matrix (ECM) by myofibroblasts has been known as an important pathological feature in IPF. Connective tissue growth factor (CTGF) is a secreted matricellular protein modulating myofibroblast activation and ECM deposition, leading to fibrosis and tissue remodeling. Protocatechuic acid is extensively distributed in many edible nuts, vegetables, and fruits and is readily absorbed by both animals and humans. Numerous biological actions of protocatechuic acid (PCA) have been observed, including antibacterial, antidiabetic, antioxidant, and anti-inflammatory characteristics. The purpose of this study is to investigate the protective effect of PCA on bleomycin-induced pulmonary fibrosis in rats. The pathological changes of the lung and levels of malondialdehyde (MDA) and glutathione (GSH) were measured. Our results revealed that PCA decreased the oxidative production of lipid MDA and increased GSH content. Moreover, PCA suppressed the expression of inflammatory biomarkers transforming growth factor β (TGF-β) and tumor necrosis factor α (TNF-α), as well as decreased collagen deposition and ECM markers alpha-smooth muscle actin (α-SMA), matrix metalloproteinase-2 (MMP-2), and metallopeptidase inhibitor 1 (TIMP-1). PCA has an anti-fibrotic effect against pulmonary fibrosis by downregulation of the CTGF/NOX4/ET-1 gene expression. Also, PCA treatment ameliorated BLM-induced lung damage by improving alveolar sac structure, reducing inflammatory cell infiltration, and preserving bronchiolar epithelial integrity, suggesting that PCA may serve as a potential treatment option for PF.
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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.