ArticleFrontiers in physiology2020
Shikonin Ameliorates LPS-Induced Cardiac Dysfunction by SIRT1-Dependent Inhibition of NLRP3 Inflammasome.
Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Yangxin Tongluo Decoction Protects Against Sepsis-Associated Cardiac Dysfunction Through Regulating Nrf2 Pathway.Mediators of inflammation · 2026Article
- Research progress in the regulatory mechanism of silent information regulator 1 in sepsis (Review).Molecular medicine reports · 2025Review
- NLRP3 Inflammasome Targeting Offers a Novel Therapeutic Paradigm for Sepsis-Induced Myocardial Injury.Drug design, development and therapy · 2025Review
- Active ingredients of traditional Chinese medicine inhibit NOD-like receptor protein 3 inflammasome: a novel strategy for preventing and treating heart failure.Frontiers in immunology · 2025Review
- Shikonin Inhibits Endoplasmic Reticulum Stress-Induced Apoptosis to Attenuate Renal Ischemia/Reperfusion Injury by Activating the Sirt1/Nrf2/HO-1 Pathway.Kidney & blood pressure research · 2025Article
- [Recent research on pyroptosis in sepsis-induced myocardial depression].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Review
- Songorine ameliorates LPS-induced sepsis cardiomyopathy by Wnt/β-catenin signaling pathway-mediated mitochondrial biosynthesis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Pharmacological Significance ofFoods (Basel, Switzerland) · 2024Review
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- Pretreatment with Indole-3-Propionic Acid Attenuates Lipopolysaccharide-Induced Cardiac Dysfunction and Inflammation Through the AhR/NF-κB/NLRP3 Pathway.Journal of inflammation research · 2024Article
- Potential biomarker for diagnosis and therapy of sepsis: Lactylation.Immunity, inflammation and disease · 2023Review
- Hydrogen sulfide alleviates lipopolysaccharide-induced myocardial injury through TLR4-NLRP3 pathway.Physiological research · 2023Article
- A bibliometric analysis of sepsis-induced myocardial dysfunction from 2002 to 2022.Frontiers in cardiovascular medicine · 2023Article
- Thymol Alleviates LPS-Induced Liver Inflammation and Apoptosis by Inhibiting NLRP3 Inflammasome Activation and the AMPK-mTOR-Autophagy Pathway.Nutrients · 2022Article
- Emodin alleviates sepsis-mediated lung injury via inhibition and reduction of NF-kB and HMGB1 pathways mediated by SIRT1.The Kaohsiung journal of medical sciences · 2022Article
- Combined Shikonin-Loaded MPEG-PCL Micelles Inhibits Effective Transition of Endothelial-to-Mesenchymal Cells.International journal of nanomedicine · 2022Article
- Molecular mechanisms and functions of pyroptosis in sepsis and sepsis-associated organ dysfunction.Frontiers in cellular and infection microbiology · 2022Review
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Pterostilbene Interferes With Lipopolysaccharide-Induced Myocardial Injury Through Oxidative Stress and Inflammasome Pathways.Frontiers in physiology · 2022Article
- l-Arginine Alleviates LPS-Induced Oxidative Stress and Apoptosis via Activating SIRT1-AKT-Nrf2 and SIRT1-FOXO3a Signaling Pathways in C2C12 Myotube Cells.Antioxidants (Basel, Switzerland) · 2021Article
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6 authors.
Funding
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Abstract
Shikonin (SHI) is an anti-inflammatory agent extracted from natural herbs. It is still unknown whether SHI ameliorates lipopolysaccharide (LPS)-induced cardiac dysfunction. This study aims to explore the protective effects of SHI on LPS-induced myocardial injury and its mechanism. The LPS-induced cardiac dysfunction mouse model was employed to investigate the protective effects of SHI. In the present study, we found that SHI treatment improved the survival rate and cardiac function and remarkably ameliorated the release of inflammatory cytokines and macrophage infiltration in heart tissue of LPS-treated mice. SHI also reduced lactate dehydrogenase (LDH) and cardiac troponin (cTn) release, cell inflammation, and apoptosis in LPS plus adenosine triphosphate (ATP)-treated H9c2 cells. In addition, SHI significantly upregulated silent information regulator 1 (SIRT1) expression and suppressed the upregulation of NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, and caspase-1 activity in heart tissues induced by LPS. Meanwhile, we got the same results in LPS plus ATP-treated H9c2 cells
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