ArticleJournal of natural medicines2024
Akebia saponin D attenuates allergic airway inflammation through AMPK activation.
Article in Journal of natural medicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 2 citations in OpenAlex.
- Obesity-related palmitic acid exacerbates IL-13-induced mucus phenotype in 16HBE airway epithelial cells via AMPK suppression.Translational pediatrics · 2026Article
- Synergistic effects of Akebia saponin D and Semaglutide on diabetic nephropathy and osteoporosis via the Klotho‑p53 signaling axis.International journal of molecular medicine · 2026Article
- Research progress on chemical metabolites, processing technologies, and pharmacological activities of asperosaponin VI: a systematic review and critical evaluation.Frontiers in pharmacology · 2026Review
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
- [Asperosaponin VI alleviates TNBS-induced Crohn's disease-like colitis in mice by reducing intestinal epithelial cell apoptosis via inhibiting the PI3K/AKT/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Akebia saponin D (ASD) is a bioactive triterpenoid saponin extracted from Dipsacus asper Wall. ex DC.. This study aimed to investigate the effects of ASD on allergic airway inflammation. Human lung epithelial BEAS-2B cells and bone marrow-derived mast cells (BMMCs) were pretreated with ASD (50, 100 and 200 μΜ) and AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) (1 mM), and then stimulated with lipopolysaccharide (LPS) or IL-33. Pretreatment with ASD and AICAR significantly inhibited TNF-α and IL-6 production from BEAS-2B cells, and IL-13 production from BMMCs. Moreover, pretreatment with ASD and AICAR significantly increased p-AMPK expression in BEAS-2B cells. Inhibition of AMPK by siRNA and compound C partly abrogated the suppression effect of ASD on TNF-α, IL-6, and IL-13 production. Asthma murine model was induced by ovalbumin (OVA) challenge and treated with ASD (150 and 300 mg/kg) or AICAR (100 mg/kg). Infiltration of eosinophils, neutrophils, monocytes, and lymphocytes, and production of TNF-α, IL-6, IL-4, and IL-13 were attenuated in ASD and AICAR treated mice. Lung histopathological changes were also ameliorated after ASD and AICAR treatment. Additionally, it showed that treatment with ASD and AICAR increased p-AMPK expression in the lung tissues. In conclusion, ASD exhibited protective effects on allergic airway inflammation through the induction of AMPK activation.
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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.