Brimonidine attenuates choroidal thinning and hypoperfusion in guinea pigs with form-deprivation myopia: Involvement of NOS and TGF-β1.

Myopia is a major public health concern that poses a serious threat to vision. The combination of precise monitoring of changes in the choroidal structure and blood flow, along with early prevention and control through pharmacological intervention, represents a key direction in myopia research. In the present study, swept-source optical coherence tomography angiography was used to obtain dynamic assessments of wide-field choroidal thickness and blood flow in guinea pigs before and after form-deprivation (FD). The effects of brimonidine on refraction, axial length, choroidal thickness, and perfusion in guinea pigs with form-deprivation myopia (FDM) were assessed. In addition, the choroidal expression of nitric oxide synthase (NOS), neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), transforming growth factor-beta1 (TGF-β1), and α-smooth muscle actin (α-SMA) was quantified. The choroidal changes observed in the guinea pigs with FDM showed spatial heterogeneity, with areas of lower baseline choroidal thickness and blood flow showing greater susceptibility to FD stimulation and exhibiting more significant reductions. Brimonidine significantly slowed refraction and axial elongation in the FDM guinea pigs and broadly alleviated choroidal thinning and hypoperfusion. At the molecular level, brimonidine markedly reduced the FD-induced elevated choroidal expression of NOS, nNOS, eNOS, TGF-β1, and α-SMA. Brimonidine showed anti-myopic effects by preserving choroidal thickness and perfusion in FDM guinea pigs, potentially through suppression of the abnormally elevated expression of NOS, TGF-β1, and α-SMA in the choroid. These findings offer new insights and therapeutic targets for pharmacological prevention and control of myopia.