ArticleFrontiers in pharmacology2021
Dihydrotanshinone I Specifically Inhibits NLRP3 Inflammasome Activation and Protects Against Septic Shock
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.Frontiers in immunology · 2026Review
- Specific inhibition of NLRP3 inflammasome by a Smurf1 inhibitorOpen medicine (Warsaw, Poland) · 2026Article
- Engineered endothelial cells targeting and dihydrotanshinone I loaded bacterial extracellular vesicles for atherosclerosis therapy.Bioengineering & translational medicine · 2025Article
- An efficient brain delivery system co-loaded with multiple components ofMaterials today. Bio · 2025Article
- Constituents fromMolecules (Basel, Switzerland) · 2024Article
- [2, 6-dimethoxy-1, 4-benzoquinone alleviates septic shock in mice by inhibiting NLRP3 inflammasome activation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Dihydrotanshinone I protects human chondrocytes and alleviates damage from spontaneous osteoarthritis in a guinea pig model.Scientific reports · 2023Article
- [Isodopharicin C inhibits NLRP3 inflammasome activation and alleviates septic shock in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Tanshinone I specifically suppresses NLRP3 inflammasome activation by disrupting the association of NLRP3 and ASC.Molecular medicine (Cambridge, Mass.) · 2023Article
- Chloride Channel and Inflammation-Mediated Pathogenesis of Osteoarthritis.Journal of inflammation research · 2022Review
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The abnormal activation of the NLRP3 inflammasome is closely related to the occurrence and development of many inflammatory diseases. Targeting the NLRP3 inflammasome has been considered an efficient therapy to treat infections. We found that dihydrotanshinone I (DHT) specifically blocked the canonical and non-canonical activation of the NLRP3 inflammasome. Nevertheless, DHT had no relation with the activation of AIM2 or the NLRC4 inflammasome. Further study demonstrated that DHT had no influences on potassium efflux, calcium flux, or the production of mitochondrial ROS. We also discovered that DHT suppressed ASC oligomerization induced by NLRP3 agonists, suggesting that DHT inhibited the assembly of the NLRP3 inflammasome. Importantly, DHT possessed a significant therapeutic effect on NLRP3 inflammasome-mediated sepsis in mice. Therefore, our results aimed to clarify DHT as a specific small-molecule inhibitor for the NLRP3 inflammasome and suggested that DHT can be used as a potential drug against NLRP3-mediated diseases.
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Registered trials
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