ArticleInflammation2025
Palmatine Attenuates Lipopolysaccharide-Induced Acute Lung Injury Via Suppression of NLRP3 Inflammasome Activation, Pyroptosis, and Metabolic Remodeling.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
- Review
- Palmatine Attenuates LPS-Induced EMT in MAC-T Cells and Mammary Fibrosis in Mice, with Suppression of NF-κB/TGF-β1/Smad Signaling In Vivo.Animals : an open access journal from MDPI · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
Acute lung injury (ALI) is a critical condition characterized by uncontrolled inflammation, respiratory insufficiency, and tissue damage, often triggered by pneumonia or sepsis. Aberrant activation of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome and subsequent pyroptosis are key drivers of ALI pathogenesis. Palmatine (PAL), a naturally derived isoquinoline alkaloid with diverse pharmacological effects, was investigated for the therapeutic potential against lipopolysaccharide (LPS)-induced ALI in this study, focusing on NLRP3 inflammasome, pyroptosis, and metabolic regulation. Our findings showed that PAL significantly suppressed NLRP3 inflammasome activation and pyroptosis in LPS/adenosine triphosphate (ATP)-stimulated THP-1 macrophages and inhibited M1 macrophage polarization. In C57BL/6J mice subjected to intratracheal LPS challenge, PAL alleviated lung histopathological injury, decreased tumor necrosis factor-α, interleukin (IL)-6, IL-1β, and IL-18 levels in bronchoalveolar lavage fluid, and reduced lung wet-to-dry ratio and lung tissue myeloperoxidase activity. Transcriptomic analysis revealed that PAL markedly attenuated LPS-induced upregulation of NLRP3 and Gasdermin-D (GSDMD). PAL also downregulated the mRNA expression of Caspase-1, Apoptosis-associated speck-like protein (Asc), High-mobility group box 1 (Hmgb1), Il1b, and Il18, as well as the protein levels of cleaved Caspase-1 (p20), GSDMD-N and Caspase-11 in lung tissue. Metabolomic profiling indicated PAL-driven metabolic reprogramming involving the oxidation of branched-chain fatty acids and very long-chain fatty acids. Integrated multi-omics analysis highlighted cytosolic DNA-sensing and NOD-like receptor signaling as key pathways underlying PAL's effects. Collectively, PAL mitigates ALI by inhibiting NLRP3 inflammasome activation, suppressing pyroptosis, and reprogramming metabolism, supporting its potential as a therapeutic candidate.
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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 OpenQuestion graph.