ArticleAmerican journal of translational research2025
Clara cell secretory protein 16 protects against PM2.5-induced ferroptosis in mouse lung epithelial cells in a concentration-dependent manner.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- CC16 alleviates PM2.5-induced airway inflammation in asthmatic mice by targeting the E-cadherin-mediated ferroptosis regulatory axis.Current research in toxicology · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Clara cell secretory protein 16 (CC16) has been reported to exert anti-inflammatory and anti-oxidant effects. However, its underlying mechanism remains unclear. This study aimed to investigate the protective effect and mechanism of CC16 using an
methodsTC-1 cells were exposed to PM2.5 to induce inflammatory injury and ferroptosis, followed by treatment with CC16 at different concentrations (0.25, 0.5, and 1.0 µg/mL). TC-1 cells were divided into six groups: control, CC16, PM2.5, PM2.5 + CC16 (0.25 μg/mL), PM2.5 + CC16 (0.5 μg/mL), and PM2.5 + CC16 (1.0 μg/mL) groups. Cell viability was assessed using the Cell Counting Kit-8 assay. Levels of inflammatory cytokines (interleukin (IL)-5, IL-6, IL-13, IL-17A, and IL-1β) in the supernatant were measured by enzyme-linked immunosorbent assay. Protein expression levels of Nrf2, ACSL4, SLC7A11, and GPX4 were detected using western blotting. Intracellular reactive oxygen species (ROS) were detected with a fluorescent probe, and mitochondrial membrane potential (MMP) was measured by JC-1 staining. Glutathione (GSH), malondialdehyde (MDA), and Fe
resultsPM2.5 exposure significantly reduced cell viability, aggravated inflammation, induced ferroptosis, and disrupted the integrity of mouse pulmonary epithelial cells. CC16 treatment reversed these effects in a concentration-dependent manner.
conclusionsCC16 effectively mitigates PM2.5-induced cellular injury in mouse pulmonary epithelial cells through inhibition of ferroptosis, with its protective effect showing a clear concentration dependence. These findings suggest CC16 as a novel strategy for PM2.5-induced respiratory disease.
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