Neuroprotective effects of lutein in a rat model of retinal detachment.

BACKGROUND: Retinal detachment (RD) is a leading cause of blindness, and although final surgical re-attachment rate has greatly improved, visual outcome in many macula-off detachments is disappointing, mainly because of photoreceptor cell death. We previously showed that lutein is anti-apoptotic in rodent models of ischemia/reperfusion injury. The objective of this study is to investigate lutein as a possible pharmacological adjunct to surgery. METHODS: Subretinal injections of 1.4 % sodium hyaluronate were used to induce RD in Sprague-Dawley rats until their retinae were approximately 70 % detached. Daily injections of corn oil (control group) or 0.5 mg/kg lutein in corn oil (treatment group) were given intraperitoneally starting 4 h after RD induction. Animals were euthanized 3 days and 30 days after RD and their retinae were analyzed for photoreceptor apoptosis and cell survival at the outer nuclear layer (ONL) using TUNEL staining and cell counting on retinal sections. Glial fibrillary acidic protein (GFAP) and rhodopsin (RHO) expression were evaluated with immunohistochemistry. Western blotting was done with antibodies against cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 to delineate lutein's mechanism of action in the apoptotic cascade. To seek a possible therapeutic time window, the same set of experiments was repeated with treatment commencing 36 h after RD. RESULTS: When lutein was given 4 h after RD, there were significantly fewer TUNEL-positive cells in ONL 3 days after RD when compared with the vehicle group. Cell counting showed that there were significantly more nuclei in ONL in lutein-treated retinae by day 30. Treatment groups also showed significantly reduced GFAP immunoreactivity and preserved RHO expression. At day 3 after RD, Western blotting showed reduced expression of cleaved caspase-3 and cleaved caspase-8 in the treatment group. No difference was found for cleaved caspase-9. When lutein was given 36 h after RD similar results were observed. CONCLUSIONS: Our results suggest that lutein is a potent neuroprotective agent that can salvage photoreceptors in rats with RD, with a therapeutic window of at least 36 h. The use of lutein in patients with RD may serve as an adjunct to surgery to improve visual outcomes.

Results of high-density silicone oil as a tamponade agent in macular hole retinal detachment in patients with high myopia.

BACKGROUND: To evaluate the use of high-density silicone oil (HDSO) as a tamponade agent for retinal detachment secondary to myopic macular hole. METHODS: 12 eyes of 12 patients with macular hole retinal detachment underwent pars plana vitrectomy, internal limiting membrane peeling and HDSO tamponade. No posturing was required postoperatively and HDSO was removed 3-4 months later. Outcome measures included macular hole closure and retinal attachment rates, best-corrected visual acuity (BCVA), and intraoperative and postoperative complications. RESULTS: The mean age of the patients was 67.8 years and the mean spherical equivalent refractive error was -13.4 diopters. After the removal of HDSO, 10 (83%) eyes had macular hole closure with retinal reattachment without any tamponade. One eye had retinal reattachment after re-operation and the other refused further surgery. At the last follow-up, the median BCVA improved from 20/800 to 20/600 (p = 0.046). A transient increase in intraocular pressure was observed in 5 (42%) eyes and one eye each developed mild oil emulsification and transient peripheral choroidal detachment. None of the eyes was found to have severe intraocular inflammation postoperatively. CONCLUSIONS: HDSO seemed to be an effective tamponade agent for myopic macular hole retinal detachment. Further prospective controlled studies seem warranted.