Purpose
To investigate the inhibitory effect of bendazol on form‐deprivation myopia (FDM) in rabbits as well as the underlying biochemical processes.
Methods
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).
Results
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 ± 0.10 mm, respectively (p < 0.001) and the VCDs were 6.56 ± 0.06, 6.69 ± 0.07 and 6.61 ± 0.06 mm, respectively (p < 0.001). HIF‐1α was upregulated in FD eyes but downregulated in FD + bendazol eyes, while the mAChRs were the opposite.
Conclusions
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.