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Noriko Yoshida, Yasuhiro Ikeda, Shoji Notomi, Keijiro Ishikawa, Yusuke Murakami, Toshio Hisatomi, Hiroshi Enaida, Tatsuro Ishibashi; Relation between Sustained Chronic Inflammatory Reaction and Oxidative Damage in an Animal Model of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2013;54(15):658.
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© ARVO (1962-2015); The Authors (2016-present)
Recent studies have suggested an inflammatory response as a possible factor in the pathogenesis of RP. In this study, we investigated the nature of retinal inflammatory response in rd10 mice, an animal model of retinitis pigmentosa (RP), and examined the effect of an antioxidant on retinal inflammation and photoreceptor apoptosis.
This study included 42 untreated rd10 mice, 30 N-acetylcysteine (NAC)-treated rd10 mice, and 20 C57BL/6 mice as controls. Real-time polymerase chain reaction (PCR) was performed to evaluate the expression levels of inflammatory factors (proinflammatory cytokines and chemokines) in rd10 mouse retinas. Rd10 mice were treated with an antioxidant NAC. Pregnant rd10 mice were given drinking water containing 7 mg/ml NAC. Then, their pups received an oral gavage of water containing 7 mg/ml NAC when they were weaned. Iits effect on retinal inflammation and photoreceptor apoptosis were examined by immunohistochemistry.
We demonstrated sequential events involving increased expression of proinflammatory cytokines and chemokines, activation of microglia, and photoreceptor apoptosis during retinal degeneration of rd10 mice. Furthermore, antioxidant treatment with NAC prevented the photoreceptor cell death along with suppression of inflammatory factors and microglial activation.
Sustained chronic inflammatory reaction may contribute to the pathogenesis of retinal degeneration in rd10 mice, suggesting interventions for ocular inflammatory reaction using antioxidants as a potential treatment for patients with RP.
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