Journal Article Ppublish
PubMed: 40155367 DOI: 10.1080/20565623.2025.2483147
Hesperidin alleviates pulmonary fibrosis by regulating EI24-mediated autophagy.
Future Sci OA 11(1):2483147
Authors: Yan Zhang, Wen Ma, Fang Wan
Affiliations
- Department of Cadre's Ward, Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China.
- Department of gerontology, Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China.
- Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guizhou Medical University, Guizhou, P.R. China.
Abstract
BACKGROUND
Etoposide-induced protein 2.4 (EI24), an essential component of autophagy, is lowly expressed in pulmonary fibrosis. Hesperidin (Hes), a flavonoid, can regulate autophagy in various diseases. However, whether Hes can inhibit pulmonary fibrosis by mechanically regulating EI24-mediated autophagy has not been uncovered.
METHODS
RLE-6TN cells were treated with transforming growth factor β1 (TGF-β1) and rats were injected with bleomycin (BLM) to construct the pulmonary fibrosis model. The effect of Hes on pulmonary fibrosis was evaluated by cell counting kit-8, immunofluorescence, hematoxylin and eosin, masson trichome staining and western blotting.
RESULTS
Hes reduced cell viability of TGF-β1-induced RLE-6TN cells. Administration of Hes restored the decrease in autophagy marker levels in TGF-β1-induced RLE-6TN cells. Hes inhibited the transcriptional and translational levels of α-SMA, collagen I and fibronectin that were increased by TGF-β1 in RLE-6TN cells. Mechanically, Hes restored EI24 expression, and EI24 knockdown reversed the effect of Hes on the expressions of autophagy and fibrosis-related proteins. Additionally, Hes enhanced autophagy and fibrosis markers, which were worsened by EI24 knockdown in BLM-induced rats.
CONCLUSION
Hes activated autophagy by upregulating EI24, which improved pulmonary fibrosis both and .
MeSH
Cells, Bleomycin, Autophagy, Fibrosis, Hesperidin, Pulmonary Fibrosis