摘要
Glutamate excitotoxicity has been postulated as a putative mechanism involved in the physiopathology of glaucoma, a disease that can cause retinal cell damage. Thus, the modulation of glutamatergic parameters is a putative therapeutic target to prevent excitotoxic retinal injury. Here, we investigated the effect of dietary omega-3 fatty acids (w3) in the retinal glutamate transport system in basal and ischemic conditions. Female Wistar rats were divided into two groups: w3 diet (w3 group) and w3 deficient-diet (D group). Their pups, at 60 days old, were used for the experiments. Retinal ischemia, a mechanism involved in the physiopathology of glaucoma, was induced by high intraocular pressure (HIOP, 140 180 mmHg for 45 min) to impair retinal blood flow. Analyses were performed 7 days after ischemia. The D group showed a decreased glutamate uptake in basal conditions and after HIOP when compared to the w3 group. After HIOP, there was a decrease in glutamate uptake in the D group that was not observed in the w3 group (p < 0.005). Concerning glutamate transporters, the w3 group presented higher levels of GLT-1 compared to the D group in basal and ischemic conditions. After HIOP, EAAC1 was increased in both groups, while GLT-1 increased only in the D group, compared to basal levels. GLAST and EAAT5 presented no alterations. The modulation of the glutamatergic system by dietary w3 fatty acids points to a potential mechanism by which w3 PUFAs exert beneficial effects in the retina.
Glutamate excitotoxicity has been postulated as a putative mechanism involved in the physiopathology of glaucoma, a disease that can cause retinal cell damage. Thus, the modulation of glutamatergic parameters is a putative therapeutic target to prevent excitotoxic retinal injury. Here, we investigated the effect of dietary omega-3 fatty acids (w3) in the retinal glutamate transport system in basal and ischemic conditions. Female Wistar rats were divided into two groups: w3 diet (w3 group) and w3 deficient-diet (D group). Their pups, at 60 days old, were used for the experiments. Retinal ischemia, a mechanism involved in the physiopathology of glaucoma, was induced by high intraocular pressure (HIOP, 140 180 mmHg for 45 min) to impair retinal blood flow. Analyses were performed 7 days after ischemia. The D group showed a decreased glutamate uptake in basal conditions and after HIOP when compared to the w3 group. After HIOP, there was a decrease in glutamate uptake in the D group that was not observed in the w3 group (p < 0.005). Concerning glutamate transporters, the w3 group presented higher levels of GLT-1 compared to the D group in basal and ischemic conditions. After HIOP, EAAC1 was increased in both groups, while GLT-1 increased only in the D group, compared to basal levels. GLAST and EAAT5 presented no alterations. The modulation of the glutamatergic system by dietary w3 fatty acids points to a potential mechanism by which w3 PUFAs exert beneficial effects in the retina.
基金
support by CAPES,FAPERGS,INCT.EN-CNPq/INCT and IBN.Net FINEP/FADESP(Proc.No.01.06.0842-00).
