ArticleScientific reports2025
Shikonin inhibits NLRP3 inflammasome activation and controls inflammatory disease.
Article in Scientific reports, 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 6 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.
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Who cites it
6 citing papers in PubMed.
- Dysregulation of the KLF9/TXNRD2 Axis Leads to Mitochondrial DNA Oxidation and NLRP3 Inflammasome Activation in Ulcerative Colitis.Journal of biochemical and molecular toxicology · 2026Article
- Integrating "Yang transforming Qi and Yin constituting the body" with immune regulation: an evidence synthesis of multidimensional traditional chinese medicine therapy for immune thrombocytopenia.Chinese medicine · 2026Review
- Shikonin Modulates the NOD2/CARD9 Pathway to Ameliorate Ulcerative Colitis Through Inhibiting M1 Macrophage Polarization.Applied biochemistry and biotechnology · 2025Article
- Impact ofJournal of inflammation research · 2025Article
- Inflammasome activation and accelerated immune aging in autoimmune disorders.Frontiers in aging · 2025Article
- Shikonin improves intestinal barrier function through modulation of GPX4 expression in intestinal epithelial cells.International journal of immunopathology and pharmacologyArticle
Corrections and comments
- Erratum issued
Authors and funding
12 authors.
Funding
Abstract
Shikonin (SHK) is a plant-derived naphthoquinone known for its anti-inflammatory activity, though the mechanism remains largely unexplored. The NLRP3 inflammasome, one of the most studied inflammasomes, can cause uncontrolled inflammation and drive various diseases when dysregulated. Here, we confirmed that SHK specifically abolished NLRP3 inflammasome activation by suppressing caspase-1 maturation and the secretion of IL-1β and IL-18. Our data demonstrated that SHK disrupted NLRP3 inflammasome assembly, primarily by blocking NLRP3 and ASC binding, thereby preventing ASC oligomerization and ASC speck formation. Furthermore, SHK reduced reactive oxygen species (ROS) production, inhibiting the generation of oxidized mitochondrial DNA (ox-mtDNA), a known inducer of NLRP3 inflammasome activation. In vivo, we showed that SHK's anti-inflammatory effect in DSS-induced ulcerative colitis (UC) and LPS-induced systemic inflammation associated with the reduction of NLRP3 inflammasome activation, as confirmed by decreased IL-1β and IL-18 release. This paper reveals the mechanism through which SHK inhibits inflammation and provides a potentially effective pharmacological strategy for treating NLRP3-related diseases.
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