Complement Activation in Retinal Degeneration

摘要: Our aim is to investigate a common role of the complement system in pathogenesis retinal disease, by assessing expression profile component 3 (C3) three mechanistically distinct models degeneration: light-damage, hyperoxia and degenerative P23H-3 rodent strain. In light damage model, young adult albino Sprague Dawley (SD) rats were exposed 1,000 lx for period up 24 h, where at specific time points during after exposure, animals euthanized retinas extracted analysis. C57 mice subjected 75% oxygen 14 days, then dissected genetic SD born reared until postnatal day 50–130, extracted. For all models, C3 mRNA levels determined quantitative PCR (qPCR), while photoreceptor death was quantified using TUNEL technique. Up-regulation evident tissue from experimental assessed. showed marked upregulation h which continued into post-exposure period. Modest increases early hyperoxia, progressed substantial days. P23H consistently higher than those non-degenerative retinas. Upregulation associated with apoptosis. While stimuli these differ, increased conjunction increasing provides evidence pathway degeneration involving activation complement.