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Review Open Access

Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review)

  • Authors:
    • Bing-Yu Liang
    • Zi-Yue Fu
    • Fen-Fen Li
    • Ping-Ting Zhou
    • Zi-Hui Xie
    • Ke Han
    • Yan-Xun Han
    • Shan-Wen Chen
    • Yi Zhao
    • Hai-Feng Pan
    • Ye-Hai Liu
    • Yu-Chen Liu
  • View Affiliations / Copyright

    Affiliations: Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230031, P.R. China, Department of Allergy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230031, P.R. China
    Copyright: © Liang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 81
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    Published online on: January 7, 2026
       https://doi.org/10.3892/mmr.2026.13791
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Abstract

Allergic rhinitis (AR) is a chronic inflammatory disorder of the nasal mucosa, often a comorbid condition with asthma, posing notable challenges for treatment. Current therapies, including corticosteroids and antihistamines, primarily target nasal symptoms but exhibit limited efficacy against concurrent asthma and systemic inflammation. Saponins, a class of bioactive plant‑derived compounds, have garnered attention for their pleiotropic effects, including immunomodulation, anti‑inflammatory activity and antioxidant properties. Saponins, such as ginsenosides, notoginsenosides, astragalosides, saikosaponins and platycodins, modulate key molecular pathways in AR, including T helper 1/2 cell balance, mast cell stabilization and NF‑κB signaling. Their multi‑target action and low toxicity profile give them advantages such as metabolic compatibility, reduced polypharmacy risks and mucosal protection. The present review highlighted the mechanistic insights into saponin‑mediated alleviation of AR and asthma, focusing on their molecular targets, signaling pathways and potential for clinical translation. The present review also discussed current limitations and future directions for the development of saponin‑based therapeutics, providing a potential foundation for novel strategies in allergic airway diseases in the future.
View Figures

Figure 1

Pathogenesis of allergic rhinitis:
Immune cell interactions and intervention points for saponins.
Allergen exposure triggers nasal epithelial cells to release
alarmins (TSLP, IL-25 and IL-33). These alarmins activate DCs and
ILC2s. DCs promote the differentiation of Th0 cells into Th2 cells,
which produce IL-4, IL-5 and IL-13. ILC2s also produce Th2-type
cytokines. IL-4 and IL-13 drive B cells to produce
allergen-specific IgE, which sensitizes MCs and basophils. Upon
subsequent allergen exposure, cross-linking of IgE triggers the
degranulation of MCs and basophils, releasing mediators (for
example, histamine, prostaglandin D2 and leukotrienes) that cause
immediate symptoms (sneezing, rhinorrhea, congestion). IL-5
recruits EOS, which release mediators such as ECP, contributing to
late-phase inflammation and tissue damage. Saponins (for example,
ginsenosides, astragalosides, saikosaponins and platycodin D)
counteract this process by: Inhibiting alarmin release; promoting
Th1/Treg differentiation; suppressing inflammatory cell activation
and degranulation; and reducing the production of key cytokines
(IL-4, IL-5, IL-13 and IgE). Red lines indicate the targeting
action of the specific saponin on the depicted pathways. Black
lines represent the signaling cascades/ cell-cell interaction.
Arrows (→) denote activation, promotion or upregulation, while
T-bars (−|) signify inhibition, suppression or downregulation. DC,
dendritic cell; EOS, eosinophil; ECP, eosinophil cationic protein;
IgE, immunoglobulin E; IL, interleukin; ILC2, innate lymphoid cell
type 2; LT, leukotriene; MC, mast cell; PAF, platelet-activating
factor; PGD2, prostaglandin D2; Th, T helper cell; Treg, regulatory
T cell; TSLP, thymic stromal lymphopoietin.

Figure 2

Pathogenic associations between
allergic rhinitis and comorbid asthma and the therapeutic
mechanisms of saponins. Associations between upper and lower airway
inflammation in the context of AR with comorbid asthma. The
neurobiology component shows nasal inflammation stimulating
trigeminal afferents associated with bronchoconstriction, with
saikosaponin A acting on this pathway. The immunology section
depicts the IgE-mediated mast cell activation cascade, Th2-driven
inflammation and the targeting of this pathway by multiple saponins
including ginsenosides and platycodin D. Physiology highlights the
anatomical continuity of airways and downward spread of
inflammation, while microbiology indicates nasal barrier disruption
and dysbiosis influencing lung environment, modulated by
ginsenoside. Red lines indicate the targeting action of the
specific saponin on the depicted pathways. Black lines represent
the signaling cascades/cell-cell interaction. Arrows (→) denote
activation, promotion or upregulation, while T-bars (−|) signify
inhibition, suppression or downregulation. AHR, airway
hyperresponsiveness; CysLTs, cysteinyl leukotrienes; DC, dendritic
cell; ECP, eosinophil cationic protein; Eos, eosinophil; IgE,
immunoglobulin E; IL, interleukin; ILC2, innate lymphoid cell type
2; LT, leukotriene; MBP, major basic protein; MC, mast cell;
MUC5AC, mucin 5AC; PG, prostaglandin; Th, T helper cell; TNF-α,
tumor necrosis factor-α; TSLP, thymic stromal lymphopoietin.

Figure 3

Molecular mechanisms of various
saponins in alleviating allergic rhinitis and comorbid asthma.
Different saponins (ginsenoside, astragaloside, platycodin D,
notoginsenoside and saikosaponin) modulate key signaling pathways
and cellular responses involved in the pathogenesis of allergic
rhinitis and asthma, leading to the amelioration of associated
symptoms (outer ring). The figure illustrates the key signaling
pathways modulated by different saponins (ginsenoside,
astragaloside, platycodin D, notoginsenoside and saikosaponin) and
the resulting amelioration of symptoms (outer ring). Ginsenoside
inhibits the RIP2/IκBβ/NF-κB axis, eosinophil activity, Th2
differentiation and the p38 MAPK pathway. Astragaloside suppresses
NF-κB activation, modulates the T-bet/GATA3 balance to inhibit Th2
responses and enhances Treg function via FoxP3. Platycodin D
inhibits p65 NF-κB and MAPK pathways, reducing IL-13, GM-CSF,
MUC5AC and eotaxin. Notoginsenoside activates Nrf2/HO-1 and AMPK
pathways, while inhibiting TNF-α/NF-κB signaling. Saikosaponin
reduces IgE/IgG1 production, inhibits Th2 and Th17 differentiation
via T-bet/GATA3 and IL-6/STAT3/ROR-γt pathways, and blocks NF-κB.
The specific mechanisms of action of these saponins are explained
in the article. Red lines indicate the targeting action of the
specific saponin on the depicted pathways. Black lines represent
the signaling cascades. Arrows (→) denote activation, promotion or
upregulation, while T-bars (−|) signify inhibition, suppression or
downregulation. Upward arrows (↑) indicate an increase and downward
arrows (↓) indicate a decrease in the respective molecule or
process. AHR, airway hyperresponsiveness; AMPK, AMP-activated
protein kinase; caspase-1, caspase-1; EOS, eosinophil; FoxP3,
forkhead box P3; GATA3, GATA binding protein 3; GM-CSF,
granulocyte-macrophage colony-stimulating factor; HO-1, heme
oxygenase-1; IgE, immunoglobulin E; IgG1, immunoglobulin G1; IκBβ,
nuclear factor of κ light polypeptide gene enhancer in B-cells
inhibitor, β; IL, interleukin; MAPK, mitogen-activated protein
kinase; MUC5AC, mucin 5AC, oligomeric mucus/gel-forming; NF-κB,
nuclear factor κ-light-chain-enhancer of activated B cells; Nrf2,
nuclear factor erythroid 2-related factor 2; p38 MAPK, p38
mitogen-activated protein kinase; RIP2, receptor-interacting
serine/threonine-protein kinase 2; ROR-γt: related orphan receptor
γt; T-bet, T-box transcription factor TBX21; Th, T helper cell;
TNF-α, tumor necrosis factor-α; Treg, regulatory T cell.
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Copy and paste a formatted citation
Spandidos Publications style
Liang B, Fu Z, Li F, Zhou P, Xie Z, Han K, Han Y, Chen S, Zhao Y, Pan H, Pan H, et al: Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review). Mol Med Rep 33: 81, 2026.
APA
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K. ... Liu, Y. (2026). Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review). Molecular Medicine Reports, 33, 81. https://doi.org/10.3892/mmr.2026.13791
MLA
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K., Han, Y., Chen, S., Zhao, Y., Pan, H., Liu, Y., Liu, Y."Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review)". Molecular Medicine Reports 33.3 (2026): 81.
Chicago
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K., Han, Y., Chen, S., Zhao, Y., Pan, H., Liu, Y., Liu, Y."Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review)". Molecular Medicine Reports 33, no. 3 (2026): 81. https://doi.org/10.3892/mmr.2026.13791
Copy and paste a formatted citation
x
Spandidos Publications style
Liang B, Fu Z, Li F, Zhou P, Xie Z, Han K, Han Y, Chen S, Zhao Y, Pan H, Pan H, et al: Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review). Mol Med Rep 33: 81, 2026.
APA
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K. ... Liu, Y. (2026). Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review). Molecular Medicine Reports, 33, 81. https://doi.org/10.3892/mmr.2026.13791
MLA
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K., Han, Y., Chen, S., Zhao, Y., Pan, H., Liu, Y., Liu, Y."Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review)". Molecular Medicine Reports 33.3 (2026): 81.
Chicago
Liang, B., Fu, Z., Li, F., Zhou, P., Xie, Z., Han, K., Han, Y., Chen, S., Zhao, Y., Pan, H., Liu, Y., Liu, Y."Therapeutic potential of saponins for allergic rhinitis: Molecular mechanisms and clinical perspectives (Review)". Molecular Medicine Reports 33, no. 3 (2026): 81. https://doi.org/10.3892/mmr.2026.13791
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