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목적 : Neurodegeneration is an important factor in diabetes-induced retinopathy since the retina is composed of a neurovascular unit. The objective of the study was to assess the influence of brimonidine, a selective α2-adrenoceptor agonist on neurodegeneration in diabetic retinopathy.
방법 : Streptozotocin was injected to trigger diabetes in rats. The rats were given one drop of 0.15% brimonidine tartrate in one eye, balanced salt solution in the other eye. Up to 8 weeks after the induction of diabetes, retinal sections were prepared for immunofluorescence staining, TUNEL assay, and western blot analysis.
결과 : Topical α2 agonist treatment decreased both apoptosis of RGC (P<0.05) and glial activation induced by diabetes. Reduction of brain-derived neurotrophic factor and phospho-Akt level after development of diabetes was blocked by brimonidine (P<0.05). Reduction of anti-apoptotic proteins (Bcl-2 and Bcl-xl) after the induction of diabetes was suppressed by brimonidine (P<0.05). Elevated p38MAPK and p53 in diabetic rats were reduced by brimonidine (P<0.05). In diabetic retinas, upregulation of the proapoptotic molecule BAX was attenuated by brimonidine treatmen (P<0.05).
결론 : α2-adrenergic activation protected RGCs through the modulation of the Akt pathway and reduction of proapoptotic p38MAPK levels in an experimental diabetic model. Topical brimonidine treatment may be another therapeutic target for neuroprotection in diabetes without the increased burden of an oral medication.
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