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H Taniguchi; Effect of FK506 on the Regulation of Apoptosis in Retinal Ischemia- reperfusion Injury . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2606.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Better treatment is needed for retinal ischemic injury. FK506 is an immunosuppressive drug that inhibits T cell receptor-mediated signal transduction. This study investigated the effect of FK506 treatment on apoptotic changes after pressure-induced ischemia-reperfusion injury in the rat retina. Methods: Wistar Kyoto rats were subjected to 60 minutes of pressure-induced ischemia, then reperfused 24 hours after pressure was released. In this study, rats were randomly divided into two groups. One group received FK506 (0.3 mg/kg weight) before reperfusion, and the other group received no treatment. The retina was examined by light and transmission electron microscopy (TEM) and in situ nick end labeling (TUNEL). Results: In the control group, significant retinal damage was observed. The cytoplasm and cytoplasmic organelles underwent progressive hydropic degeneration including swelling and vacuolation. Apoptotic findings were shown with the TUNEL method and TEM. Apoptotic cells were more prominent in the inner and outer nuclear layer. In the FK506-treated group, apoptotic cell death and inflammation decreased, showing that FK506 was beneficial in the preservation of the retina. Conclusions: Our study demonstrates that FK506 prevented apoptosis in retinal ischemia- reperfusion injury. The effects of FK506 on apoptosis in the retina are described for the first time, and these findings suggest that it can improve retinal circulation. FK506 may act at the level of DNA and may have potential therapeutic applications in diseases involving apoptosis.
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