Perinatal asphyxia induces retinal lesions, generating ischemic proliferative retinopathy which may result in blindness. Previously, we showed that the nitrergic system was involved in the physiopathology of perinatal asphyxia. Here we analyze the application of methylene blue, a well-known soluble guanylate cyclase inhibitor, as a therapeutic strategy to prevent retinopathy. Male rats (n=28 per group) were treated in different ways: 1) CTL (control) group comprised born to term animals; 2) PA group comprised rats exposed to perinatal asphyxia (20 min., at 37ºC); and 3) MB-PA group comprised animals born from pregnant rats treated with methylene blue (2 mg/kg) 30 and 5 min before delivery and then the pups were subjected to PA as above. mRNA was obtained at different times after asphyxia for molecular studies and tissue was collected at 30 days for morphological and biochemical analysis. Perinatal asphyxia produced significant gliosis, angiogenesis, and thickening of the inner retina. Methylene blue treatment reduced these parameters. Perinatal asphyxia resulted in a significant elevation of the nitrergic system as shown by NOS activity assays, Western blotting and (immuno)histochemistry for nNOS and NADPH-diaphorase activity. All these parameters were also normalized by the treatment. In addition, methylene blue induced the upregulation of the antiangiogenic peptide, PEDF. Application of methylene blue reduced morphological and biochemical parameters of retinopathy. This finding suggests the use of methylene blue as a new treatment to prevent or decrease retinal damage in the context of ischemic proliferative retinopathy.
- Nitric oxide
- Ischemic proliferative retinopathy
- Methylene blue
- Copyright © 2015, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology