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Network Pharmacology and Experimental Research of β-Sitosterol in Treating Chronic Obstructive Pulmonary Disease via the Glucocorticoid Receptor.

Created on 19 Aug 2026

Authors

Xiaohong Deng, Tianhao Wang, Jianying Wang, Kun Wang

Published in

Journal of visualized experiments : JoVE. Issue 234. Aug 07, 2026. Epub Aug 07, 2026.

Abstract

Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disorder characterized by persistent inflammation, oxidative stress, and progressive lung function decline. The therapeutic potential of β-sitosterol in COPD remains unclear. This study aimed to investigate the protective effects of β-sitosterol against COPD and elucidate its underlying mechanism. Database screening identified the glucocorticoid receptor (GR) as a potential target of β-sitosterol. A cigarette smoke-induced COPD mouse model and a cigarette smoke extract (CSE)-stimulated BEAS-2B cell model were established. Pulmonary function, lung injury-related markers, inflammation, oxidative stress, and cellular senescence were assessed using (RT-qPCR), DCFH-DA fluorescent probe assays, and senescence detection kits. The effects of β-sitosterol alone or in combination with dexamethasone (DEX) were also evaluated. β-sitosterol significantly improved pulmonary function, normalized lung injury-related markers, and attenuated inflammation, oxidative stress, and cellular senescence in both CSE-stimulated BEAS-2B cells and cigarette smoke-exposed mice. These protective effects were accompanied by increased GR expression. Moreover, β-sitosterol enhanced responsiveness to DEX, and combined treatment with β-sitosterol and DEX produced greater improvements in pulmonary function, lung injury markers, inflammation, reactive oxygen species levels, and cellular senescence than DEX treatment alone. Collectively, these findings suggest that β-sitosterol alleviates COPD-associated pathological changes, at least in part, by upregulating GR expression and enhancing the therapeutic efficacy of DEX, highlighting its potential as an adjuvant strategy for COPD treatment.

PMID:
42611937
Bibliographic data and abstract were imported from PubMed on 19 Aug 2026.

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