Minocycline does not inhibit microglia proliferation or neuronal regeneration in the facial nucleus following crush injury
Minocycline does not inhibit microglia proliferation or neuronal regeneration in the facial nucleus following crush injury
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DOI：
10.1016/j.neulet.2005.05.047
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发表时间：
2005-09-16
影响因子：
2.5
通讯作者：
Streit, WJ
中科院分区：
文献类型：
--
作者：
Fendrick, SE;Miller, KR;Streit, WJ
米诺环素被认为是通过抑制与神经退行性疾病相关的神经炎症(小胶质细胞激活)而起到神经保护作用。在这项研究中，我们研究了米诺环素对神经挤压伤后面神经核内小胶质细胞有丝分裂活性和神经元再生的影响。于术后第2、3、4天用H-3-胸腺嘧啶核苷标记分裂的小胶质细胞，并对面神经核内标记细胞进行计数。用荧光金标记再生神经元，观察损伤后7、14、21d运动神经元的再生模式。损伤后各时间点的小胶质细胞和荧光金标记神经元比较，二甲胺四环素治疗组与对照组无明显差异。研究结果表明，即使在高水平的米诺环素存在的情况下，小胶质细胞仍能在体内保持激活的能力。(C)2005爱思唯尔爱尔兰有限公司。保留所有权利。
Minocycline is thought to be neuroprotective by inhibiting neuroinflammation (microglial activation) associated with neurodegenerative diseases. In this study we investigated the effect of minocycline specifically on microglial mitotic activity and neuronal regeneration within the facial nucleus following a nerve crush injury. Proliferation was measured by labeling the dividing microglia with H-3-thymidine and quantifying labeled cells throughout the facial nucleus on days 2, 3 and 4 post-axotomy. Regeneration patterns of the axotomized motoneurons were studied by labeling regenerating neurons with fluorogold at 7, 14 and 21 days post-axotomy. No significant difference was found between minocycline treated and control rats when comparing the 3H-thymidine labeled microglial cells or fluorogold labeled neurons at these post-injury time points. The findings show that microglia maintain the ability to become activated in vivo even in the presence of high levels of minocycline. (c) 2005 Elsevier Ireland Ltd. All rights reserved.