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R. Garg, R. Sanchez, C.K. Chan, S. Garg, M.J. Wong, A.A. Sadun, T.T. Lam; Interleukin-10 (IL-10) after Ischemia Reperfusion Injury to the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2930.
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Introduction: We have previously showed that IL-10 changes after ischemia-reperfusion (I/R) injury to the rat retina. To further characterize the role of IL-10 after I/R injury, we localized IL-10 and evaluated the possible neuroprotective effect of IL-10 in the retina. Methods: Cannulas, connected to a saline column that generated a pressure of 110 mmHg, were inserted into the anterior chambers of Adult Lewis albino rats. The elevated pressure was maintained for 1 hour to render the retina ischemic and reperfusion was established after the ischemic period. Groups of animals were then euthanized at 0, 4, 12, 18 or 48 hours post reperfusion and their eyes were enucleated. The retinas were fixed, processed, and embedded in paraffin for sectioning. Immunohistochemistry was performed using anti-IL-10 (n=3) antibody. Other groups of animals were subjected to I/R injury and received intravitreal injections of 0 (n=5), 1 (n=4), 3 (n=7), 10 (n=8) or 30 (n=7) ng IL-10. These animals were euthanized 7 days after I/R injury, their retinas were flat mounted and the number of RGC’s was counted. Results: There was very little IL-10 immunoreactivity in normal retinas. However, IL-10 was localized to cells that resembled microglia in the inner nuclear layer at 18 and 48 hours after I/R injury. Unexpectedly, our pharmacologic study showed that intravitreal administration of IL-10 had no significant effect on the number of RGC’s when compared to vehicle treated retinas. Conclusion: There is IL-10 immunoreactivity in microglia-like cells in the inner retina at a late stage after I/R injury. Its role in neuroprotection/neurodegeneration is not clear and remains to be further examined.
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