Purpose: Hydrogen sulfide (H2S), a colorless gas, has been confirmed to be a gaseous messenger molecule and an endogenous stimulus for angiogenesis recently. This study was performed to investigate the role of H2S in diabetic retinopathy.
Methods: Blood samples were collected from normal controls and patients with diabetes. Vitreous samples were collected from patients with proliferative diabetic retinopathy (PDR) and patients with rhegmatogenous retinal detachment. Patients were grouped into diabetic patients without diabetic retinopathy (non-DR), with nonproliferative DR, and with PDR. Concentrations of H2S and vascular endothelial growth factor in the plasma and vitreous body were detected using a spectrophotometer.
Results: A decreased H2S level in the plasma was observed in non-DR group (41.89 ± 8.52 μM, P < 0.05), and an increased H2S level in the plasma was observed in PDR group (60.49 ± 11.14 μM, P < 0.001), when compared with that in normal controls (49.67 ± 9.72 μM). There was no difference in plasma H2S level between patients with nonproliferative DR (54.13 ± 8.61 μM) and normal controls. In the vitreous body, H2S levels in PDR group were significantly higher (76.80 ± 24.08 μM, P < 0.001) than that in rhegmatogenous retinal detachment group (24.37 ± 11.25 μM). Levels of vascular endothelial growth factor in plasma from patients with diabetes were significantly lower (P < 0.001) than that in normal controls. Vascular endothelial growth factor levels in the vitreous body from diabetic patients with PDR were significantly higher (885.61 ± 190.41 pg/mL, P < 0.001) than that from patients with rhegmatogenous retinal detachment (89.98 ± 19.56 pg/mL). Seven days after an intravitreal injection of ranibizumab, a significantly decreased H2S level (55.58 ± 7.20 μM, P < 0.05) was observed in the vitreous body in patients with PDR when compared with that (75.07 ± 12.95 μM) in the vitreous body collected just before intravitreal injection.
Conclusion: These results indicated that anti-vascular endothelial growth factor may downregulate the H2S level in the vitreous body, and H2S may play a role in the development of DR. Hydrogen sulfide may be a novel target for the therapy of DR.