Aldose reductase‐deficient mice were protected from the neuro‐retinal injury after carotid artery transient ischemia

Previously, we showed that AR deficiency prevents retinal abnormalities in 15 mos. diabetic db/db mice. Here, we explored the role of AR in ischemic retinal injury, since the retinal damage associated with diabetes is thought to be the consequence of ischemia. To induce retinal ischemia, we blocked the ophthalmic artery, which gives rise to central retinal artery, by using 2 hrs of internal carotid artery occlusion and 22 hrs of reperfusion by intraluminal insertion of filament. Here, we compared the ipsilateral retina of 8 wks old AR‐wild type (AR +/+ ) to the similar aged AR −/− mice after transient ischemia. After the transient ischemia, there was a significant increase of total retinal thickness and neuronal cell loss in the ipsilateral side of AR +/+ retinas, but not of the AR −/− retinas when compared with the contralateral sides, respectively. Increase of neuro‐retinal damage after the transient ischemia triggered the increased expression of glutamine synthetase, which was shown to protect against neuronal degeneration in injured retinal tissues, and markers of glial reactivation, such as glial acidic fibrillary protein (GFAP) and S‐100 in Müller cells in the ipsilateral side of AR +/+ , but not of the AR −/− retinas, when compared with the contralateral sides, respectively. This suggests that AR deficiency prevents neuro‐retinal damage and glial reactivation induced by the carotid artery transient ischemia. This research was supported by Research Grants Council of Hong Kong Grant to Dr. S.K. Chung.