The studies were applied in three di erent groups (control, PA and MB) of 30 postnatal day animals. The studies were performed in retina by using enzymatic activity, NADPHd histochemical method and immunohistochemistry against nNOS. isoform of the enzyme nitric oxide sinthase (nNO) as trigger of the structural and molecular alterations previously observed by our group of research, and analyzing the application of methylene blue (MB) a therapeutic strategy. Studying the participation of nitric oxide (NO) through the neuronal. Furthermore, we have identified the involvement of the nitregic system in it physiopatology. Previously, we have demonstrated retinal neurodegeneration, gliosis and neovascularization. Hipoxia-ischemia by perinatal asphyxia (PA) is cause of retinal lesions, and can produce blindness by ischemic proliferative retinopathy (IPR). This finding stimulates future studies aiming to use MB as a new treatment to avoid or decrease retinal damage in the context of ROP. Application of MB as a therapeutic strategy showed a strong effect inhibiting constitutive NOS activity and nNOS expression. Histochemical and immunohistochemical studies support these results, with nNOS localization in ganglionar and amacrine cells. 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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January 2023
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