ArticleFrontiers in immunology2017
Baicalin Inhibits NOD-Like Receptor Family, Pyrin Containing Domain 3 Inflammasome Activation in Murine Macrophages by Augmenting Protein Kinase A Signaling.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- The NLRP3 Inflammasome: Mechanisms of Activation, Regulation, and Therapeutic Opportunities.MedComm · 2026Review
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Flavonoids regulating NLRP3 inflammasome: a promising approach in alleviating diabetic peripheral neuropathy.Inflammopharmacology · 2025Review
- Lithospermic acid targeting heat shock protein 90 attenuates LPS-induced inflammatory response via NF-кB signalling pathway in BV2 microglial cells.Immunologic research · 2025Article
- Baicalin inhibits PANoptosis by blocking mitochondrial Z-DNA formation and ZBP1-PANoptosome assembly in macrophages.Acta pharmacologica Sinica · 2025Article
- Selenized Tripterine Phytosomes Alleviate Ferroptosis-Mediated Acute Kidney Injury by Suppressing GPX4 Degradation via the DUSP1/Autophagy Pathway.Biomaterials research · 2025Article
- Immuno-modulatory role of baicalin in atherosclerosis prevention and treatment: current scenario and future directions.Frontiers in immunology · 2024Review
- The dance of macrophage death: the interplay between the inevitable and the microenvironment.Frontiers in immunology · 2024Review
- Theaflavin mitigates acute gouty peritonitis and septic organ injury in mice by suppressing NLRP3 inflammasome assembly.Acta pharmacologica Sinica · 2023Article
- Baicalein Suppresses NLRP3 and AIM2 Inflammasome-Mediated Pyroptosis in Macrophages Infected by Mycobacterium tuberculosis via Induced Autophagy.Microbiology spectrum · 2023Article
- Gout-associated monosodium urate crystal-induced necrosis is independent of NLRP3 activity but can be suppressed by combined inhibitors for multiple signaling pathways.Acta pharmacologica Sinica · 2022Article
- Mechanistic Insights on the In Vitro Antibacterial Activity and In Vivo Hepatoprotective Effects ofPharmaceuticals (Basel, Switzerland) · 2022Article
- Concurrent suppression of Aβ aggregation and NLRP3 inflammasome activation for treating Alzheimer's disease.Chemical science · 2022Article
- Baicalin Alleviates Contrast-Induced Acute Kidney Injury Through ROS/NLRP3/Caspase-1/GSDMD Pathway-Mediated Proptosis in vitro.Drug design, development and therapy · 2022Article
- Hidden Agenda - The Involvement of Endoplasmic Reticulum Stress and Unfolded Protein Response in Inflammation-Induced Muscle Wasting.Frontiers in immunology · 2022Review
- Morphine enhances LPS-induced macrophage apoptosis through a PPARγ-dependent mechanism.Experimental and therapeutic medicine · 2021Article
- Detecting Critical Functional Ingredients Group and Mechanism of Xuebijing Injection in Treating Sepsis.Frontiers in pharmacology · 2021Article
- Triclabendazole Induces Pyroptosis by Activating Caspase-3 to Cleave GSDME in Breast Cancer Cells.Frontiers in pharmacology · 2021Article
- Inhibition of NLRP3 Inflammasome Activation and Pyroptosis in Macrophages by Taraxasterol Is Associated With Its Regulation on mTOR Signaling.Frontiers in immunology · 2021Article
- Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The flavonoid baicalin has been reported to possess potent anti-inflammatory activities by suppressing inflammatory signaling pathways. However, whether baicalin can suppress the activation of NOD-like receptor (NLR) family, pyrin containing domain 3 (NLRP3) inflammasome in macrophages is largely unknown. Here, we showed that baicalin treatment dose-dependently inhibited adenosine triphosphate (ATP) or nigericin-induced NLRP3 inflammasome activation, as revealed by the decreased release of mature interleukin (IL)-1β, active caspase-1p10, and high-mobility group box-1 protein from lipopolysaccharide (LPS)-primed bone marrow-derived macrophages. The formation of ASC specks, a critical marker of NLRP3 inflammasome assembly, was robustly inhibited by baicalin in the macrophages upon ATP or nigericin stimulation. All these inhibitory effects of baicalin could be partly reversed by MDL12330A or H89, both of which are inhibitors of the protein kinase A (PKA) signaling pathway. Consistent with this, baicalin strongly enhanced PKA-mediated phosphorylation of NLRP3, which has been suggested to prevent ASC recruitment into the inflammasome. Of note, the PKA inhibitor H89 could block baicalin-induced NLRP3 phosphorylation on PKA-specific sites, further supporting PKA's role in this process. In addition, we showed that when administered pre and post exposure to
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