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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Antioxidants reduce cone cell death in a model of retinitis pigmentosa
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Antioxidants reduce cone cell death in a model of retinitis pigmentosa

机译：抗氧化剂可减少色素性视网膜炎模型中的锥体细胞死亡

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Retinitis pigmentosa (RP) is a label for a group of diseases caused by a large number of mutations that result in rod photoreceptor cell death followed by gradual death of cones. The mechanism of cone cell death is uncertain. Rods are a major source of oxygen utilization in the retina and, after rods die, the level of oxygen in the outer retina is increased. In this study, we used the rd1 mouse model of RP to test the hypothesis that cones die from oxidative damage. A mixture of antioxidants was selected to try to maximize protection against oxidative damage achievable by exogenous supplements; a-tocopherol (200 mg/kg), ascorbic acid (250 mg/kg), Mn(III)tetrakis (4-benzoic acid) porphyrin (10 mg/kg), and a-lipoic acid (100 mg/kg). Mice were treated with daily injections of the mixture or each component alone between postnatal day(P)18 and P35. Between P18 and P35, there was an increase in two biomarkers of oxidative damage, carbonyl adducts measured by ELISA and immunohistochemical staining for acrolein, in the retinas of rd1 mice. The staining for acrolein in remaining cones at P35 was eliminated in antioxidant-treated rd1 mice, confirming that the treatment markedly reduced oxidative damage in cones; this was accompanied by a 2-fold increase in cone cell density and a 50% increase in medium-wavelength cone opsin mRNA. Antioxidants also caused some preservation of cone function based upon photopic electroretinograms. These data support the hypothesis that gradual cone cell death after rod cell death in RP is due to oxidative damage, and that antioxidant therapy may provide benefit.
机译：色素性视网膜炎（RP）是由大量突变引起的一组疾病的标签，这些突变导致视杆光感受器细胞死亡，然后视锥逐渐死亡。视锥细胞死亡的机制尚不确定。视杆是视网膜中氧气利用的主要来源，视杆死亡后，视网膜外层的氧气水平增加。在这项研究中，我们使用RP的rd1小鼠模型测试了视锥细胞因氧化损伤而死亡的假说。选择一种抗氧化剂混合物以尝试最大程度地保护其免受外源性补品所能达到的氧化损伤。 α-生育酚（200 mg / kg），抗坏血酸（250 mg / kg），Mn（III）四（4-苯甲酸）卟啉（10 mg / kg）和α-硫辛酸（100 mg / kg）。在出生后第（P）18至P35天之间每天对混合物或每种成分单独注射治疗。在P18和P35之间，在rd1小鼠的视网膜中，氧化损伤的两个生物标志物，通过ELISA测定的羰基加合物和对丙烯醛的免疫组织化学染色有所增加。在抗氧化剂处理过的rd1小鼠中，P35其余视锥细胞中的丙烯醛染色被消除，从而证实该处理显着降低了视锥细胞的氧化损伤。这伴随着视锥细胞密度增加了2倍，中波长视锥视蛋白mRNA增加了50％。抗氧化剂还基于视神经视网膜电图使锥体功能得以保留。这些数据支持以下假设：RP中杆状细胞死亡后锥体细胞逐渐死亡是由于氧化损伤，抗氧化剂治疗可能会带来益处。

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