Neuroprotective effect of NecroX-5 against retinal degeneration in rodents.

NecroX-5 is a derivative of cyclopentylamino carboxymethylthiazolylindole (NecroX), an inhibitor of necrosis/necroptosis. NecroX-5 has been shown to scavenge mitochondrial reactive oxygen and nitrogen species, and thus preventing necrotic cell death against various kinds of oxidative stress in several tissues, including the brain. To examine the effect of NecroX-5 on retinal degeneration (RD), RD was induced in Sprague-Dawley rats by an intraperitoneal injection of N-methyl-N-nitrosourea and in BALB/c mice by blue light-emitting diode exposure. Scotopic electroretinography recording was used to evaluate retinal function. For histological evaluation, hematoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP nick end labeling, and immunohistochemistry were performed. Electroretinography recordings showed that a-waves and b-waves were significantly reduced in both RD rats and mice, whereas the amplitudes of both waves were significantly increased in both NecroX-5-treated RD rats and mice compared with untreated RD animals. In hematoxylin and eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, the outer nuclear layer where photoreceptors reside appeared to be more preserved, and there were fewer apoptotic cells in NecroX-5-treated RD retinas than in untreated RD retinas. In addition, immunohistochemistry with antiglial fibrillary acidic protein and anti-8-hydroxy-2'-deoxyguanosine showed lower levels of retinal injury and oxidative stress in NecroX-5-treated RD retinas than in untreated RD retinas. These results indicated that NecroX-5 protects retinal neurons from experimentally induced RD, suggesting that NecroX-5 may have a potential for the treatment of RD as a medication.

Cyanidin-3-glucoside extracted from mulberry fruit can reduce N-methyl-N-nitrosourea-induced retinal degeneration in rats.

PURPOSE: To investigate the effect of cyanidin-3-O-glucoside (C3G) on a rat retinal degeneration (RD) model. MATERIALS AND METHODS: Experimental RD was induced in rats by the intraperitoneal injection of N-methyl-N-nitrosourea (MNU) at 50 mg/kg. C3G extracted from mulberry (Morus alba L.) fruit (50 mg/kg) was orally administered, daily for 1, 2 and 4 weeks after MNU injection. The effects of C3G administration on MNU-induced RD retinas were histologically and functionally assessed by hematoxylin and eosin staining and electroretinography (ERG), respectively. The degree of retinal injury in C3G-administered RD rats was evaluated by immunohistochemistry with an antibody against glial fibrillary acidic protein (GFAP). The preferential protective effect of C3G on scotopic vision was examined by western blot analysis. RESULTS: Marked loss of photoreceptors in the outer nuclear layer (ONL) was observed in RD rats at 2 and 4 weeks after MNU injection, while the ONL in the MNU-induced RD rats given C3G was relatively well preserved. Immunohistochemistry with anti-GFAP showed that retinal injury was also reduced in the retinas of the rats given C3G. Functional assessment by using ERG recordings showed that scotopic ERG responses were significantly increased in RD rats given C3G for 4 weeks (p < 0.01) compared with that of untreated RD rats. In the RD rats given short-term C3G (for 1 and 2 weeks), the increase in ERG responses was not significant. In addition, western blot analysis showed that rhodopsin level in the C3G-administered RD retinas significantly increased compared to that in the non-administered RD retinas (p < 0.05), whereas red/green opsin level did not show any significant difference. CONCLUSIONS: Long-term administration of C3G extracted from mulberry fruit could structurally reduce photoreceptor damage and functionally improve scotopic visual functions in the RD rat model induced by MNU.

Effect of cataract surgery on the progression of diabetic retinopathy.

PURPOSE: To study the effect of cataract surgery and other factors on the progression of diabetic retinopathy using the nonoperated contralateral eye as a control. SETTING: Department of Ophthalmology, Catholic University Medical College, Uijongbu St. Mary's Hospital, Seoul, Korea. METHODS: Monocular cataract surgery was performed in 75 patients who had the same degree of retinopathy or no retinopathy in both eyes preoperatively. Patients were assigned to 1 of 2 groups as follows: Group A, progression of retinopathy in the operated eye caused by cataract surgery; Group B, no progression of retinopathy bilaterally, comparable level of progression in both eyes, or more progression of retinopathy in the nonoperated eye than in the operated eye. The differences between the 2 groups in age, duration of and treatment methods for diabetes, renal function, and presence of preoperative macular edema were compared. The 1-year follow-up included evaluation of the progression of retinopathy. RESULTS: Surgery caused the retinopathy to progress in 23 patients (30.6%, Group A); 52 patients (69.4%, Group B) had no progression of retinopathy or a comparable level of retinopathy postoperatively. The operated eye had more progression of retinopathy than the nonoperated contralateral eye (P <.05). There was no significant difference between the 2 groups in age, diabetes duration, surgical method, or hypertension. Preoperative macular edema and poor renal function significantly affected the progression of diabetic retinopathy after cataract surgery (P <.05). CONCLUSIONS: Diabetic retinopathy progressed after cataract surgery. The presence of preoperative macular edema and poor renal function increased the progression of retinopathy postoperatively.