Minocycline inhibition of photoreceptor degeneration.
Minocycline inhibition of photoreceptor degeneration.
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DOI：
10.1001/archophthalmol.2009.288
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发表时间：
2009-11
影响因子：
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通讯作者：
Liu Yang;Joon-Hyun Kim;Kyle D. Kovacs;J. Arroyo;D. Chen
中科院分区：
文献类型：
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作者：
Liu Yang;Joon-Hyun Kim;Kyle D. Kovacs;J. Arroyo;D. Chen
目的探讨米诺环素对实验性视网膜脱离（retinal detachment，RD）感光细胞的保护作用。方法采用1.4%透明质酸钠溶液诱导小鼠视网膜脱离模型。在一项实验中，小鼠每天接受米诺环素（第1组）或盐水（第2组）注射。在第二个实验中，在实验RD之前24小时、之后立即或之后24小时开始用米诺环素或盐水处理小鼠。在这两个实验中，感光细胞的存活和凋亡进行了评估，通过免疫组织化学与感光细胞标志物，视杆视紫红质，视锥细胞视蛋白的一级抗体，并通过末端脱氧核苷酸转移酶介导的dUTP-生物素末端标记。结果实验性视网膜脱离后第1天可见光感受器细胞凋亡，第3天凋亡细胞数量达到高峰，第7天凋亡细胞数量下降。在RD前24小时或RD后24小时给予米诺环素治疗可显著减少与RD相关的凋亡感光细胞数量。结论：我们的数据表明，米诺环素可能是有用的，在与RD相关的感光细胞变性的治疗，即使在RD后24小时给药。临床相关性在黄斑脱离型RD患者中使用米诺环素可预防感光细胞凋亡和神经胶质细胞增殖，改善最终视力结果。
OBJECTIVE To determine whether systemic minocycline can protect photoreceptors in experimental retinal detachment (RD). METHODS Retinal detachment was induced in mice by subretinal injection of sodium hyaluronate, 1.4%. In 1 experiment, mice received daily injections of minocycline (group 1) or saline (group 2). In a second experiment, mice were treated with minocycline or saline beginning 24 hours prior, immediately after, or 24 hours after experimental RD. In both experiments, photoreceptor cell survival and apoptosis were assessed by immunohistochemistry with primary antibodies against photoreceptor cell markers, rod rhodopsin, and cone opsin, and by terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling. RESULTS Photoreceptor cell apoptosis was detected at day 1 after experimental RD, with apoptotic cells peaking in number at day 3 and dropping by day 7. Treatment with minocycline significantly reduced the number of apoptotic photoreceptor cells associated with RD when given 24 hours before or even 24 hours after RD. CONCLUSIONS Our data suggest that minocycline may be useful in the treatment of photoreceptor degeneration associated with RD, even when given up to 24 hours after RD. CLINICAL RELEVANCE Use of minocycline in patients with macula-off RD may prevent photoreceptor apoptosis and glial cell proliferation, improving final visual outcomes.