Topical bendazol inhibits experimental myopia progression and decreases the ocular accumulation of HIF-1α protein in young rabbits.

Abstract

To investigate the inhibitory effect of bendazol on form-deprivation myopia (FDM) in rabbits as well as the underlying biochemical processes. Forty-eight 3-week-old New Zealand white rabbits were randomly assigned to three groups: a control group, a form-deprivation (FD) group and an FD+bendazol group (treated with 1% bendazol in the FD eyes). Refraction, corneal curvature, vitreous chamber depth (VCD) and axial length (AL) were assessed using streak retinoscopy, keratometry, and A-scan ultrasonography, respectively. Eyeballs were enucleated for histological analysis, and ocular tissues were homogenized to determine the mRNA and protein expression of hypoxia-inducible factor-1α (HIF-1α) and muscarinic acetylcholine receptors (mAChRs). Bendazol inhibited the progression of FDM and suppressed the upregulation of HIF-1α. At week 6, in the control, FD and FD+bendazol groups, the refraction values were 1.38±0.43, 0.03±0.47 and 1.25±0.35 D, respectively (p<0.001); the ALs were 13.91±0.11, 14.15±0.06 and 13.97±0.10mm, respectively (p<0.001) and the VCDs were 6.56±0.06, 6.69±0.07 and 6.61±0.06mm, respectively (p<0.001). HIF-1α was upregulated in FD eyes but downregulated in FD+bendazol eyes, while the mAChRs were the opposite. In the FD rabbit model, bendazol significantly inhibits the development of myopia and downregulates HIF-1α expression, which may provide a novel therapeutic approach for myopia control.