ArticleCurrent research in toxicology2026
Protective role of calcitriol in PM2.5-induced apoptosis and inflammation in bronchial epithelial cells
Article in Current research in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
PM2.5 contributes to lung injury by inducing oxidative stress, inflammatory responses, and apoptosis. Calcitriol exerts a protective role against lung injury by regulating the vitamin D receptor (VDR) and Nrf2 signaling pathways, mitigating PM2.5-induced oxidative stress and inflammation. In this study, we investigated the protective effects of calcitriol against PM2.5-induced apoptosis, oxidative damage, and inflammation in human bronchial epithelial BEAS-2B cells, with a specific focus on the crosstalk between VDR and Nrf2 signaling. BEAS-2B cells were pre-treated with calcitriol (1, 10, 100 nM) for 24 h before PM2.5 exposure (100 µg/mL). Apoptosis, DNA damage, and inflammation were assessed by flow cytometry, ELISA, qRT-PCR, and Western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate VDR-antioxidant response element (ARE) binding. Calcitriol suppressed apoptotic signaling by reducing p53 phosphorylation and downregulating the mRNA expression of
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