Agardh Carl-David, Hultberg Björn, Nayak Ramesh C, Farthing-Nayak Pamela, Agardh Elisabet
Department of Endocrinology, University Hospital MAS, Malmö, Sweden.
Antioxid Redox Signal. 2005 Nov-Dec;7(11-12):1486-93. doi: 10.1089/ars.2005.7.1486.
Diabetic retinopathy is a sight-threatening complication of diabetes, and loss of pericytes represents early signs of its development. We tested the hypothesis that high glucose levels may induce signs of oxidative stress in cultured bovine retinal pericytes. Pericytes were exposed to either normal (5.5 mM) or high (22 mM) glucose levels for 1, 3, and 5 days. Signs of oxidative stress were measured by expression of copper/zinc superoxide dismutase, manganese superoxide dismutase, catalase, and glutathione peroxidase using real-time RTPCR. To elucidate the role of oxidative stress, we also measured glutathione (GSH) concentration in the cells and investigated the impact of thiol-reactive metal ions and hydrogen peroxide (H(2)O(2)) on intracellular GSH. Despite the stimulation with high glucose, thiol-reactive metal ions, or H(2)O(2), there was no clear increased expression of antioxidant enzymes or influence of GSH levels. Lipid peroxidation (malondialdehyde level) was increased in bovine aortic smooth muscle cells, but not in bovine retinal pericytes. The data indicate that pericytes do not develop oxidative stress in response to hyperglycemia. However, it is not definitively excluded that oxidative stress may occur after longer time periods of glucose stimulation.
糖尿病视网膜病变是糖尿病一种威胁视力的并发症,周细胞的丢失是其发展的早期迹象。我们检验了高血糖水平可能在培养的牛视网膜周细胞中诱导氧化应激迹象的假设。将周细胞分别暴露于正常(5.5 mM)或高(22 mM)葡萄糖水平下1天、3天和5天。通过实时逆转录聚合酶链反应检测铜/锌超氧化物歧化酶、锰超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的表达来测量氧化应激迹象。为阐明氧化应激的作用,我们还测量了细胞中的谷胱甘肽(GSH)浓度,并研究了硫醇反应性金属离子和过氧化氢(H₂O₂)对细胞内GSH的影响。尽管用高血糖、硫醇反应性金属离子或H₂O₂刺激,抗氧化酶的表达没有明显增加,GSH水平也没有受到影响。牛主动脉平滑肌细胞中的脂质过氧化(丙二醛水平)增加,但牛视网膜周细胞中未增加。数据表明周细胞不会因高血糖而产生氧化应激。然而,不能完全排除在葡萄糖刺激更长时间后可能会发生氧化应激。