ArticleMediators of inflammation2015
Astragaloside IV inhibits NF- κ B activation and inflammatory gene expression in LPS-treated mice.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 93 citations in OpenAlex.
- Effects of Niaoduqing Particles () on Delaying Progression of Renal Dysfunction: A Post-trial, Open-Label, Follow-up Study.Chinese journal of integrative medicine · 2019Trial
- Efficacy and Safety of Niaoduqing Particles for Delaying Moderate-to-severe Renal Dysfunction: A Randomized, Double-blind, Placebo-controlled, Multicenter Clinical Study.Chinese medical journal · 2017Trial
- Astragaloside IV confers vascular protection after traumatic brain injury through an Nrf2-dependent mechanism involving VWF.IBRO neuroscience reports · 2026Article
- Mechanisms of Action of Herbal Preparations for the Rehabilitation of Dust-Related Diseases of the Bronchopulmonary System.Biomedicines · 2026Review
- A Bioactive PLGA-modified SIS scaffold loaded with astragaloside IV-preconditioned BMSCs promotes infected wound healing.Scientific reports · 2026Article
- Diet and Medicinal Herbs as Adjunctive Approaches to Immune Homeostasis in Sjögren's Disease.International journal of molecular sciences · 2026Review
- Validating Natural Compounds as Toll-Like Receptor 4 (TLR4) Antagonists: Experimental Challenges and Therapeutic Perspectives.Journal of medicinal chemistry · 2026Review
- Therapeutic Targets, Pharmacological Mechanisms, and Delivery Strategies for Diabetic Peripheral Neuropathy.Drug design, development and therapy · 2026Review
- Natural Compounds Targeting Coronary Microvascular Dysfunction: Mechanisms and Beyond.Drug design, development and therapy · 2026Review
- Astragaloside IV ameliorates DSS-induced intestinal epithelial barrier dysfunction associated with modulation of tight junction proteins and MLCK/p-MLC and MyD88/TRAF6 signaling pathways.Frontiers in pharmacology · 2026Article
- Osteoimmunomodulation of astragalus-calcium silicate scaffolds-activated M2 macrophage-derived miR-218-rich exosome for enhanced bone regeneration.Materials today. Bio · 2025Article
- [Astragaloside IV alleviates D-GAL-induced endothelial cell senescence by promoting mitochondrial autophagyNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Novel pyrrolo[2,1-RSC advances · 2025Article
- Role of Cellular Senescence in Parkinson's Disease: Potential for Disease-Modification Through Senotherapy.Biomedicines · 2025Review
- Astragaloside IV mitigates influenza-induced inflammatory responses by suppressing the Wnt/β-catenin signalling pathway in alveolar macrophages.Veterinary research · 2025Article
- Prospects for the Protective Mechanisms and Compounds of Bufei Huoxue Capsule against COVID-19 Convalescence: Evaluation of Integrating UHPLC-HRMS Analysis and Network Pharmacology Strategy.Combinatorial chemistry & high throughput screening · 2025Article
- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
- Article
- Astragaloside IV as a promising therapeutic agent for liver diseases: current landscape and future perspectives.Frontiers in pharmacology · 2025Review
- Jiawei Shengjiangsan's Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In this study we investigated the role of astragaloside IV (AS-IV), one of the major active constituents purified from the Chinese medicinal herb Astragalus membranaceus, in LPS-induced acute inflammatory responses in mice in vivo and examined possible underlying mechanisms. Mice were assigned to four groups: vehicle-treated control animals; AS-IV-treated animals (10 mg/kg b.w. AS-IV daily i.p. injection for 6 days); LPS-treated animals; and AS-IV plus LPS-treated animals. We found that AS-IV treatment significantly inhibited LPS-induced increases in serum levels of MCP-1 and TNF by 82% and 49%, respectively. AS-IV also inhibited LPS-induced upregulation of inflammatory gene expression in different organs. Lung mRNA levels of cellular adhesion molecules, MCP-1, TNFα, IL-6, and TLR4 were significantly attenuated, and lung neutrophil infiltration and activation were strongly inhibited, as reflected by decreased myeloperoxidase content, when the mice were pretreated with AS-IV. Similar results were observed in heart, aorta, kidney, and liver. Furthermore, AS-IV significantly suppressed LPS-induced NF-κB and AP-1 DNA-binding activities in lung and heart. In conclusion, our data provide new in vivo evidence that AS-IV effectively inhibits LPS-induced acute inflammatory responses by modulating NF-κB and AP-1 signaling pathways. Our results suggest that AS-IV may be useful for the prevention or treatment of inflammatory diseases.
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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 OpenQuestion graph.