Astragaloside IV suppresses histamine-induced inflammatory factors and mucin 5 subtype AC overproduction in nasal epithelial cells via regulation of inflammation-related genes

ABSTRACT

Allergic rhinitis (AR) is a symptomatic allergic disease that leads to severe inflammation. Astragaloside IV (AS-IV) is a primary active component of Astragalus membranaceus and exerts immune-regulation and anti-inflammatory effects. However, the pharmacological effect of AS-IV in the nasal epithelial cells (NECs) has not been reported. The present study aimed to assess the effect of AS-IV on inflammatory cytokines and mucin 5 subtype AC (MUC5AC) overproduction in histamine (His)-stimulated NECs and its underlying mechanism. NECs were stimulated with or without His for 24 h in the absence or presence of AS-IV. The levels of inflammatory cytokines including IL-6, IL-8, MCP-1, IL-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), eotaxin, and MUC5AC were assayed. Our findings indicated that AS-IV inhibited His-evoked release and expression of inflammatory cytokines and MUC5AC in NECs. RNA-seq analyses indicated the significant changes in expression levels involved in inflammation genes upon treatment of His-induced NECs with AS-IV. Our findings indicated that AS-IV inhibited His-evoked inflammatory cytokines secretion and MUC5AC overproduction in NECs, which were partly mediated by regulation of inflammation-related genes. Therefore, our findings provided a scientific basis for the development of AS-IV as an effective agent for clinical therapeutic strategy in the treatment of AR.

KEYWORDS:

• Antihistamine
• nasal mucosa
• allergic rhinitis
• muc5ac
• inflammatory cytokine
• rna-seq

Highlights

(1) AS-IV may be considered a novel drug for the treatment of AR.

(2) AS-IV inhibits His-induced inflammation in NECs.

(3) AS-IV inhibits MUC5AC overproduction of NECs induced by His.

(4) AS-IV regulates inflammation-related genes in His-stimulated NECs.

Acknowledgements

The manuscript has been submitted as a preprint in Research Square in the below link: https://www.researchsquare.com/article/rs-520631/v1.

Disclosure statement

The authors declare that they have no competing interests.

Data Availability Statement

The datasets generated for this study are available on request to the corresponding author.

Additional information

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.