ArticleMolecular medicine (Cambridge, Mass.)2023
Tanshinone I specifically suppresses NLRP3 inflammasome activation by disrupting the association of NLRP3 and ASC.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Unraveling potent therapeutic potentials of tanshinones, lipophilic abietane diterpenes: a holistic literature review.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Screening of Natural Product-Derived USP7 Inhibitors for Cancer Therapy via Integrated Machine Learning and Molecular Simulations.Current issues in molecular biology · 2026Article
- Research progress on the molecular mechanisms of tanshinone IIA in the treatment of cardiovascular and cerebrovascular diseases (Review).International journal of molecular medicine · 2026Review
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Phytotherapy in precision medicine era: deciphering herbal modulation of multi-omic biomarkers for cardiovascular metabolic syndrome remodeling.Frontiers in medicine · 2026Article
- Multimodal modulation of metal-based nanomaterials in osteoarthritis immunotherapy: current landscape and future paradigms.Frontiers in immunology · 2026Review
- Bidirectional Regulation of NLRP3 Inflammasome and Mitochondrial Quality Control in Sepsis: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- An efficient brain delivery system co-loaded with multiple components ofMaterials today. Bio · 2025Article
- Understanding a Potential Role for the NLRP3 Inflammasome in Placenta-Mediated Pregnancy Complications.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Network pharmacology-based study on the mechanism of Tangfukang formula against type 2 diabetes mellitus.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Tanshinone I Ameliorates Psoriasis-Like Dermatitis by Suppressing Inflammation and Regulating Keratinocyte Differentiation.Drug design, development and therapy · 2025Article
- New applications of clioquinol in the treatment of inflammation disease by directly targeting arginine 335 of NLRP3.Journal of pharmaceutical analysis · 2025Article
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Peritoneal fibrosis: from pathophysiological mechanism to medicine.Frontiers in physiology · 2024Review
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbnormal activation of NLRP3 inflammasome is related to a series of inflammatory diseases, including type 2 diabetes, gouty arthritis, non-alcoholic steatohepatitis (NASH), and neurodegenerative disorders. Therefore, targeting NLRP3 inflammasome is regarded as a potential therapeutic strategy for many inflammatory diseases. A growing number of studies have identified tanshinone I (Tan I) as a potential anti-inflammatory agent because of its good anti-inflammatory activity. However, its specific anti-inflammatory mechanism and direct target are unclear and need further study.
methodsIL-1β and caspase-1 were detected by immunoblotting and ELISA, and mtROS levels were measured by flow cytometry. Immunoprecipitation was used to explore the interaction between NLRP3, NEK7 and ASC. In a mouse model of LPS-induced septic shock, IL-1β levels in peritoneal lavage fluid and serum were measured by ELISA. Liver inflammation and fibrosis in the NASH model were analyzed by HE staining and immunohistochemistry.
resultsTan I inhibited the activation of NLRP3 inflammasome in macrophages, but had no effect on the activation of AIM2 or NLRC4 inflammasome. Mechanistically, Tan I inhibited NLRP3 inflammasome assembly and activation by targeting NLRP3-ASC interaction. Furthermore, Tan I exhibited protective effects in mouse models of NLRP3 inflammasome-mediated diseases, including septic shock and NASH.
conclusionsTan I specifically suppresses NLRP3 inflammasome activation by disrupting the association of NLRP3 and ASC, and exhibits protective effects in mouse models of LPS-induced septic shock and NASH. These findings suggest that Tan I is a specific NLRP3 inhibitor and may be a promising candidate for treating NLRP3 inflammasome-related diseases.
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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.