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Proteomic analysis of rat retina in a steroid-induced ocular hypertension model: potential vulnerability to oxidative stress.

机译:在类固醇诱发的高眼压模型中大鼠视网膜的蛋白质组学分析:潜在的氧化应激脆弱性。

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PURPOSE: To investigate global protein expression profiles in the retinas of normal and glucocorticoid-induced ocular hypertensive rats by proteomic analysis. METHODS: Ocular hypertension was induced by topical application of dexamethasone (DEX) for 4 weeks. Age-matched untreated rats served as controls. Intraocular pressure (IOP) was monitored by an electronic tonometer. Retinal protein expression profiling was carried out by two-dimensional fluorescence difference gel electrophoresis (2-D DIGE). Proteins were identified by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry. RESULTS: In DEX-treated rats, average IOP was elevated significantly compared with controls. With DEX treatment, levels of four proteins were altered, as revealed by 2-D DIGE and MALDI-TOF mass spectrometry: apolipoprotein A1 (apoA1), a lipid-binding protein, upregulated 1.9-fold, P < 0.05; alpha A crystallin (CRYAA), a molecular chaperone, downregulated 2.7-fold, P < 0.01; superoxide dismutase 1 (SOD1), an antioxidant enzyme, downregulated 2.3-fold, P < 0.05; and triosephosphate isomerase 1 (TPI1), a glycolytic enzyme, downregulated 2.3-fold, P < 0.01. CONCLUSIONS: Downregulation of CRYAA, SOD1, and TPI1, observed here after a short period of DEX-induced ocular hypertension, may be involved in the onset of neural damage in steroid-induced glaucoma.
机译:目的:通过蛋白质组学分析调查正常和糖皮质激素诱发的眼高血压大鼠视网膜的整体蛋白表达谱。方法:局部应用地塞米松(DEX)4周可诱发高眼压。年龄匹配的未处理大鼠作为对照。通过电子眼压计监测眼内压(IOP)。通过二维荧光差异凝胶电泳(2-D DIGE)进行视网膜蛋白表达谱分析。通过基质辅助激光解吸电离飞行时间(MALDI-TOF)质谱鉴定蛋白质。结果:在接受DEX治疗的大鼠中,平均IOP与对照组相比显着提高。通过2-D DIGE和MALDI-TOF质谱分析,DEX处理改变了四种蛋白质的水平:载脂蛋白A1(apoA1),一种脂质结合蛋白,上调了1.9倍,P <0.05。 αA晶体蛋白(CRYAA),一种分子伴侣,下调2.7倍,P <0.01;超氧化物歧化酶1(SOD1),一种抗氧化酶,下调2.3倍,P <0.05;糖酵解酶磷酸三糖异构酶1(TPI1)下调了2.3倍,P <0.01。结论:在短暂的DEX诱导的高眼压后短时间内观察到的CRYAA,SOD1和TPI1的下调可能与类固醇诱导的青光眼神经损伤的发作有关。

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