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Article Abstract
Aim: To investigate whether nintedanib can inhibit pterygium cells through the fibroblast growth factor receptor 2 (FGFR2)/extracellular-signal-regulated kinase (ERK) pathway.
Methods: Human primary pterygium cells were cultured . After treatment with nintedanib, the cell morphology was observed under microscopy, the morphological changes of the nucleus were observed after DAPI staining, apoptosis was analyzed by Annexin-V FITC/PI double staining, and the changes of apoptosis-associated proteins were detected by Western blot. The binding ability of nintedanib to FGFR2 was predicted by molecular docking. Finally, by silencing FGFR2, we explored whether nintedanib inhibited FGFR2/ERK pathway.
Results: The results showed that nintedanib inhibited the growth of pterygium cells and caused nuclear pyknosis. The results of Annexin-VFITC/PI double staining showed that nintedanib was able to induce early and late apoptosis of pterygium cells, significantly increasing the expression of apoptosis-associated proteins Bax and cleaved-Caspase3 (<0.05), and reducing the expression of Bcl-2 (<0.05). In addition, nintedanib significantly inhibited ERK1/2 phosphorylation through FGFR2 (<0.05). After silencing the expression of FGFR2, there was no significant difference in the inhibition of ERK1/2 phosphorylation by nintedanib (>0.05).
Conclusion: Nintedanib induces apoptosis of pterygium cells by inhibiting FGFR2/ERK pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10089899 | PMC |
| http://dx.doi.org/10.18240/ijo.2023.04.03 | DOI Listing |
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