STC-1 alleviates airway inflammation by regulating epithelial cell apoptosis through the 5-LO pathway
- PMID: 39546157
- DOI: 10.1007/s10753-024-02181-5
STC-1 alleviates airway inflammation by regulating epithelial cell apoptosis through the 5-LO pathway
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 (TGF- ), 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.
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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
-
- 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
-
- 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
-
- 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
-
- 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
-
- 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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