ArticleHeliyon2023
Saikosaponin D inhibits nasal inflammation by regulating the transcription factors T-box protein expressed in T cells/GATA-3 and retinoic acid-related orphan nuclear receptor γt in a murine model of allergic rhinitis.
Article in Heliyon, 2023. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Saikosaponin D Attenuates Postherpetic Neuralgia and Reduces Inflammation by Regulating Gut Microbiota in a Rodent Model.Biochemical genetics · 2026Article
- Th17/Treg cell imbalance in allergic rhinitis: mechanisms and therapeutic implications.Genes and immunity · 2026Review
- Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review).Molecular medicine reports · 2026Review
- Exploring the Therapeutic Potential ofPharmaceuticals (Basel, Switzerland) · 2025Review
- Saikosaponin D Inhibits Lung Metastasis of Colorectal Cancer Cells by Inducing Autophagy and Apoptosis.Nutrients · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Context: Saikosaponin D (SSD) is a commonly prescribed agent against inflammatory diseases in Asian countries. However, the anti-allergic inflammatory effect of SSD in allergic rhinitis (AR) model is not well known. Objective: We investigated the anti-allergic and anti-inflammatory effects of SSD on the ovalbumin (OVA)-induced AR model. Materials and method: BALB/c mice were divided into the control, OVA, OVA + SSD, and OVA + dexamethasone (Dex) groups. AR was established by intraperitoneal injection with OVA adsorbed to aluminum hydroxide, and intranasal challenge with OVA. Thereafter, the mice were treated with 10 mg/kg BW (Body weight) of OVA + SSD and 2.5 mg/kg BW of Dex orally for 11 days before being challenged. Subsequently, the mice were challenged with OVA 1 h after SSD or Dex treatment. The Control group was treated with saline only. Results: The addition of 10 mg/kg BW of OVA + SSD significantly ameliorated the nasal symptoms including sneezing and rubbing from 30 ± 5.2 times in OVA group to 20 ± 5.8 times. Moreover, OVA + SSD group decreased the production of TNF-α, IL-4, IL-5, IL-17, GATA-3 and RORγ about 1.2-1.4-fold compared to the OVA-induced AR mice near to 2.5 mg/kg BW of Dex levels. Meanwhile OVA + SSD group slightly increased the levels of INF-γ, IL-12 and T-bet about 1.8-2.0-fold compared to the OVA group near to control group. Notably, OVA + SSD group also reduced the levels of OVA-specific IgE and IgG1 about 0.5-2.5-fold compared OVA group but increased the levels of IgG2a in serum. The results were analyzed using Graph Pad Prism software (v5.0, La Jolla, CA, USA). Conclusion: SSD may represent an alternative therapeutic approach for the treatment of patients with AR through the regulation of transcription factors T-bet, GATA-3, and RORγ in inflammatory cells.
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