Molecular mechanism of fluoroquinolones modulation on corneal fibroblast motility.

摘要: Topical fluoroquinolones are widely used to prevent ocular infections after ophthalmic surgery. However, they have been shown affect the corneal cell motility, whose mechanism remains indefinite. The purpose of this study was investigate how stromal motility. Human fibroblasts (HCFs) were incubated in ciprofloxacin (CIP), levofloxacin (LEV), or moxifloxacin (MOX) at 0, 10, 50, and 100 μg/ml for up 3 days. Effect CIP, LEV, MOX on HCF migration monitored using assay. viability determined by WST-1 Expression focal adhesion kinase (FAK), paxillin (PXN), their phosphorylated forms analyzed immunoblotting. Binding affinity between FAK PXN co-immunoprecipitation. Our results revealed that CIP MOX, but not noticeably retarded migration. proliferation significantly reduced (38.2%), LEV (29.5%), (21.3%), respectively (p = 0.002). suppressed phosphorylation tyrosines (10.2 ± 4.3%, p < 0.001; 11.7 ± 2.4%, p < 0.001, respectively), including tyrosine 118 (33.3 ± 5.2%, 34.0 ± 4.4%, respectively). diminished binding (8.2 ± 1.8%, 9.0 ± 4.5%, Nevertheless, dephosphorylation dissociation found LEV-treated HCFs. None these FAK-Y397. We conclude might delay fibroblast via interfering with recruitment adhesions tyrosines.