| Objective:To develop a simple model of retinal detachment and reattachment in rats without damaging vitreous and inner limiting membrane and observe the effects of pro-inflammatory cytokines in experimental retinal detachment and reattachment. Methods:1. Histopathology (Hematoxylin and eosin-stain, HE), retrograde label method and transmission electron microscope were applied to observe the proliferative procession both in detached and reattached neuro-retina, the loss of ganglion cell, the change of nerve fiber layer and the breakdown of inner blood-retinal barrier in detached retina.2. The level of IL-1β , IL-6, IL-8, TGF-# and TNF-# in neuro- retina at various period after retinal detachment were measured with radio-immune method, and the expresson of IL-1β, IL-6, IL-8, TGF-# , TNF-# in neuro-retina and retinal pigment epithelial cells both in detached and reattached retina were located with monoclonal or polyclonal antibody by immunohistochemistry.3. The loss of RGCs during retinal detachment and reattachment were measured by the count of RGCs retrogradely labeled by FluoroGold, and to ascertain the main role of IL-1β contributed to RGC loss and the neuro-protective effect of IL-1Ra by treatment with IL-1β antibody and IL-1Ra. Proliferating cell nuclear antigen (PCNA) as a indicator of proliferation in neuro-retina and RPE cells was measured with flowcytometry. to illustrate the proliferating effect of IL-1β in experimental retinal detachment and it's cause with the intervention of anti-IL-1β with IL-Ra and IL-1β antibody. Results:1. The animal model of experimental retinal detachment without damaging inner limiting membrane and vitreous are successfully conducted in rats. The separation of neuro-retina and RPE could only result in subretinal proliferation.2. RGCs loss was observed in detached retina ,and reached to its peak at 1day after retinal detachment, then continued at a low level as long as the retina detached. Early reattachment could stop the loss of RGCs. Delayed reattachment could increase the loss of RGCs. Blocking the main pro-inflammation cytokine could reduce the loss of RGCs during experimental retinal detachment.3.The expression of PCNA began at the second day and reached a maximum at about 10 days, then declined and continued at a low level as long as the retina detached. IL-1β antibody and IL-1Ra could partially lower the expression of PCNA . High expression of PCNA could be induced by exogenous IL-1β.4. Pro-inflammation cytokine, such as IL-1β, IL-6, IL-8, over-expressed during retinal detachment , and could be lowered by reattachment.5. Blood-retinal barrier breakdown was due to endogenous pro-inflammation cytokine.Conclusions:1. The animal model of separation between neuro-retina and RPEis successfully produced and could eliminate the influence of othercomplicated factors. It enable us to investigate the sequel mainly due tothe separation of neuro-retina with RPE.2.The separation of neuro-retina and RPE initiated proliferating process, andresulted sub-retinal proliferation, but no evidennce of epiretinal proliferationwas found.3.After retinal detachment, RGCs loss was in the manner of apoptosis andcorrelated with the time lengh of detachment. IL-1β played a main role inRGCs loss and early reattachment could stop further RGC loss.4. Endogenous pro-inflammatory cytokine was contributed to the BRB breakdown.5. The separation of neuro-retina and RPE could induce the over expression of pro-inflammatory cytokine both in neuro-retina and RPE directly. Reattachment could lower the expression.6. The simple separation of neuro-retina and RPE could increase the expression of both pro-inflammatory cytokine and PCNA, and the expression peak of pro-inflammatory cytokine was just preceding that of PCNA. Exogenous pro-inflammatory cytokine could also increase the expression of PCNA in detached retina, while the expression of PCNA could be...
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