Prevention of ischemia-reperfusion caused apoptosis in rat retinas by captopril and iloprost

In this study, we aimed at studying antioxidant and antiapoptotic properties ofcaptopril and iloprost in ischemic rat retina by using immunohistochemistry. Captopril is aninhibitor of angiotensin converting enzyme which is widely used for regulation ofcardiovascular and renal functions. Iloprost is a synthetic prostacyclin which hascytoprotective effects, and leads to vasodilation in blood vessels. Despite the fact that anumber of studies have focused on tissue protective effects of both drugs in myocardial andendothelial cells, antiapoptotic properties of both captopril and iloprost during retinalischemia-reperfusion injury remain unclear.To determine antiapoptoric properties of captopril and iloprost, a 30-minute ishemiafollowed by a 90-minute reperfusion was created by bilateral ligation and release of carotidarteries. During this process, captopril and iloprost were injected. Retinal tissue collectedfrom euthanized animals were subjected to immunohistochemistry. Caspase 8, 9 , and 3activities were measured. Evaluation of stained tissues were performed under lightmicroscopy.In comparison to controls, ischemia-reperfusion resulted in a severe injury in retinaltissues as assessed by increased caspase activities in all caspases tested. Captopril inhibiteddramatically activity of caspase-8 whereas it did not have any effect on caspase-9 dependentpathway of apoptosis. In contrast, ilprost decreased remarkably activities of all three caspases.In conclusion, our results indicated that while iloprost may protect and rescue retinafrom apoptosis, protection of captopril was only partial, and may not rescue retinal tissuesfrom apoptosis as a result of ischemia-reperfusion injury. In this respect, iloprost may beprefered as a drug of choise in treatment of retinal diseases. However, extensive studies arealso required to make a final conclusion.