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. 2025 Aug;48(4):2152-2165.
doi: 10.1007/s10753-024-02181-5. Epub 2024 Nov 15.

STC-1 alleviates airway inflammation by regulating epithelial cell apoptosis through the 5-LO pathway

Affiliations

STC-1 alleviates airway inflammation by regulating epithelial cell apoptosis through the 5-LO pathway

Shijia Wang et al. Inflammation. 2025 Aug.

Abstract

Airway inflammation plays a key role in the pathogenesis and development of asthma. Stanniocalcin-1 (STC-1) has powerful antioxidant, anti-inflammatory and anti-apoptotic functions but its impact on the airway inflammation in asthma lacks evidence. Here, we investigated the effect and potential mechanism of STC-1 on airway inflammation through asthmatic mice model and lipopolysaccharide (LPS)-treated BEAS-2B cells. The data showed that STC-1 treatment before the challenge exerted protective effect on ovalbumin (OVA)-induced asthmatic mice, i.e., decreased the inflammatory cell infiltration, mucus secretion, cytokine levels, apoptosis levels, and p38 MAPK signaling. Additionally, STC-1 reduced 5-LO expression. Meanwhile, STC-1 decreased p38 MAPK signaling, cytokine production, mucin MUC5AC production, 5-LO expression and nuclear translocation, and LTB4 production in vitro. Ultimately, transforming growth factor β (TGF- β ), as a 5-LO inducer, reversed the anti-inflammatory and anti-apoptotic effects of STC-1 in BEAS-2B cells by up-regulating 5-LO expression. It reveals the potential of STC-1 to act as an additional therapy to mitigate airway inflammation in asthma and inhibit 5-LO expression.

Keywords: Airway inflammation; Apoptosis; Asthma; Stanniocalcin-1.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests. Ethical approval: The animal study protocol was reviewed and approved by the Laboratory Animal Center of the First Affiliated Hospital of Wenzhou Medical University (WYYYIACUCAEC2023038).

References

    1. Papi, A., C. Brightling, S.E. Pedersen, and H.K. Reddel. 2018. Asthma. The Lancet 391 (10122): 783–800. https://doi.org/10.1016/s0140-6736(17)33311-1 . - DOI
    1. El-Husseini, Z.W., R. Gosens, F. Dekker, and G.H. Koppelman. 2020. The genetics of asthma and the promise of genomics-guided drug target discovery. The Lancet Respiratory Medicine 8 (10): 1045–1056. https://doi.org/10.1016/s2213-2600(20)30363-5 . - DOI - PubMed
    1. McIntyre, A., and W.W. Busse. 2022. Asthma exacerbations: the achilles heel of asthma care. Trends in Molecular Medicine 28 (12): 1112–1127. https://doi.org/10.1016/j.molmed.2022.09.001 . - DOI - PubMed - PMC
    1. Comhair, S.A., and S.C. Erzurum. 2010. Redox control of asthma: molecular mechanisms and therapeutic opportunities. Antioxidants & Redox Signaling 12 (1): 93–124. https://doi.org/10.1089/ars.2008.2425 . - DOI
    1. Michaeloudes, C., H. Abubakar-Waziri, R. Lakhdar, K. Raby, P. Dixey, I.M. Adcock, S. Mumby, P.K. Bhavsar, and K.F. Chung. 2022. Molecular mechanisms of oxidative stress in asthma. Molecular Aspects of Medicine 85: 101026. https://doi.org/10.1016/j.mam.2021.101026 . - DOI - PubMed

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