ArticleEndocrine, metabolic & immune disorders drug targets2025
Tanshinone IIA Regulates NRF2/NLRP3 Signal Pathway to Restrain Oxidative Stress and Inflammation in Uric Acid-Induced HK-2 Fibrotic Models.
Article in Endocrine, metabolic & immune disorders drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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
8 citing papers in PubMed.
- Tanshinone IIA suppresses cancer metastasis by modulating tumor cell-platelet-endothelial cell interactions.Oncology letters · 2026Article
- Tanshinone IIA attenuates psoriasis via Nrf2/HO-1 activation: Mechanistic insights from preclinical models.Biochemistry and biophysics reports · 2026Article
- Advances in Nanotechnology-Assisted Delivery of TCM-Derived Bioactive Compounds for Wound Repair.Pharmaceutics · 2026Review
- Review
- The multifaceted mechanisms of Tanshinone IIA in doxorubicin-induced cardiotoxicity.Frontiers in medicine · 2026Review
- Wuling capsule alleviates hyperuricaemia and protects UA- injured HK-2 cells by regulating uric acid transporter proteins.Frontiers in pharmacology · 2025Article
- Harnessing the therapeutic value of Tanshinone IIA: a breakthrough therapy in cardiovascular diseases.Frontiers in pharmacology · 2025Review
- Natural products in traditional Chinese medicine for renal fibrosis: a comprehensive review.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
introductionThis study aims to investigate the function and potential mechanism of Tanshinone IIA in uric acid-induced HK-2 fibrosis models. MATERIALS AND
methodsAn
resultsTanshinone IIA inhibited the increase in inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-18 and the formation of NLRP3 inflammasome induced by uric acid stimulation. In addition, Tanshinone IIA treatment reduced the production of ROS and MDA, promoting the expression of SOD and CAT, thereby protecting HK-2 cells from oxidative stress damage. Besides, the expression of TGF-β, FN, and Collagen I was significantly reduced by the treatment of Tanshinone IIA. Mechanistically, Tanshinone IIA inhibited the expression of inflammatory cytokines and the formation of the NLRP3 inflammasome by targeting NRF2.
conclusionTanshinone IIA exerts a protective role in uric acid-induced HK-2 fibrosis models by targeting the NRF2-NLRP3 signaling pathway to reduce the occurrence of inflammation and oxidative stress.
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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.