Inhibition of nNOS and COX-2 expression by lutein in acute retinal ischemia

• Published in: Nutrition (Burbank, Los Angeles County, Calif.) Los Angeles County, Calif.), 2006-06, Vol.22 (6), p.668-671
• Main Authors: Choi, Jun-Sub, Kim, Dongmyung, Hong, Yeon-Mi, Mizuno, Satoshi, Joo, Choun-Ki
• Format: Article
• Language: English
• Subjects: Acute Disease; Animals; Antioxidants; Apoptosis; Biological and medical sciences; Cyclo-oxygenase–2; Cyclooxygenase 2 - metabolism; Cyclooxygenase 2 Inhibitors - pharmacology; Dose-Response Relationship, Drug; Eye - blood supply; Eye - enzymology; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Injections, Intraperitoneal; Ischemia; Ischemia - enzymology; Laboratory animals; Light microscopy; Lutein; Lutein - pharmacology; Macular degeneration; Medical research; Medical sciences; Mortality; Neuronal nitric oxide synthase; Nitric oxide; Nitric Oxide Synthase - metabolism; Ophthalmology; Proteins; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Retina; Retina - enzymology; Retina - metabolism; Retinopathies; Rodents; Studies; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Vitreous Body
• ISSN: 0899-9007; 1873-1244
• DOI: 10.1016/j.nut.2005.08.011

Lutein is a major nutrient in the retina. Lutein has an antioxidative effect and protects against macular degeneration and retinal degenerative disease. However, the mechanism of lutein is not clear in retinal degeneration, and a role for lutein is not known in ischemic injury. In this study, an ischemia-induced rat retina was examined to determine the effect of the lutein on ischemic retinal cell death. We used a transient ischemia model of high intraocular pressure in the rat. Lutein (Kemin Foods, LC) was injected into the intraperitoneal or intravitreous before ischemia. Retinal degeneration was observed by light microscopy 24 h after ischemia. Expressions of neuronal nitric oxide synthase (nNOS) and cyclo-oxygenase–2 (COX-2) were detected by western blot analysis at various times after retinal ischemia. The nNOS and COX-2 expression levels were increased early in ischemic control retinas, but these increases were inhibited by lutein. In addition, the inhibitory effect of lutein was observed to be dose dependent. Further, ischemia-induced cell death was inhibited by lutein. Lutein-injected ischemic retina appeared similar to normal retina. This study investigated the protective effect of lutein on retinal ischemia and the inhibitory effect of nNOS and COX-2 expressions. These results suggest that a supplement with lutein may have the potential to inhibit ischemic cell death by this mechanism in the neural retina.