![]() CTL with a significant 60% reduction in PA+MB vs. This was correlated with a 28% significant increment in nNOS expression in PA vs. ![]() A significant increase of nNOS activity was observed in retinas of 30 day-old animals subjected to PA compared to CTL (PA=10,8☐,4 CTL=9,1☐,3 pmol/min/mg protein, p<0,05), while PA+MB animals showed no Constitutive NOS enzymatic activity, NADPH diaphorase histochemical method, immunohistochemistry and Western-blot assay for nNOS were used to evaluate retinas. We used 30 days-old male Spregue-Dawley rats (n=5/group) obteined as follows: 1) PA were animals exposed to perinatal asphyxia (20min, at 37☌), 2) PA+MB were animals born from pregnant to term female rats treated with MB (2mg/kg) 30 and 5min before delivery and subjected to PA induction during 20min at 37☌, 3) CTL were born to term animals. We hypothetize the participation of nitric oxide (NO) through the neuronal isoform of the enzyme nitric oxide synthase (nNOS) as trigger of the previously observed structural and molecular alterations, and analyze the application of methylene blue (MB), a NOS inhibitor, as a therapeutic strategy. ![]() ![]() Furthermore we have identified the involvement of the nitrergic system in this physiopathology. Previously we have demonstrated in this model retinal neurodegeneration, gliosis, and neovascularization, which are compatible with retinopathy of prematuriry (ROP). Perinatal asphyxia is able to induce retinal lesions, generating ischemic proliferative retinopathy (IPR) resulting, in severe cases, in blindness.
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