Direct protection of cultured neurons from ischemia-like injury by minocycline.
Direct protection of cultured neurons from ischemia-like injury by minocycline.
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DOI：
10.5115/acb.2010.43.4.325
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发表时间：
2010-12
影响因子：
1.1
通讯作者：
Yenari MA
中科院分区：
文献类型：
--
作者：
Huang WC;Qiao Y;Xu L;Kacimi R;Sun X;Giffard RG;Yenari MA
米诺环素是一种四环素抗生素，现在已知可以通过抗炎机制保护细胞。我们使用神经元缺血样损伤的体外模型进一步探讨了这种效应。与单独的神经元相比，将神经元与小胶质细胞（大脑的常驻免疫细胞）共培养，会适度增加因缺氧和葡萄糖剥夺（OGD）而导致的细胞死亡。用米诺环素处理共培养物可将细胞死亡降低至显着低于单独神经元的水平。用米诺环素或各种免疫介质抑制剂处理共培养物，也导致细胞死亡减少。重要的是，用组织纤溶酶原激活剂、基质金属蛋白酶、TNF-α和诱导型一氧化氮合酶以及米诺环素的相同抑制剂处理不添加小胶质细胞的神经元培养物也导致细胞死亡减少。因此，抗炎治疗似乎可以直接保护神经元免受体外缺血的影响。
Minocycline, a tetracycline antibiotic, is now known to protect cells via an anti-inflammatory mechanism. We further explored this effect using an in vitro model of ischemia-like injury to neurons. Coculturing neurons with microglia, the brain's resident immune cell, modestly increased cell death due to oxygen and glucose deprivation (OGD), compared to neurons alone. Treatment of cocultures with minocycline decreased cell death to a level significantly lower than that of neurons alone. Treatment of cocultures with minocycline or inhibitors of various immune mediators, also led to decreased cell death. Importantly, treatment of neuron cultures without added microglia with these same inhibitors of tissue plasminogen activator, matrix metalloproteinases, TNF-alpha and inducible nitric oxide synthase as well as minocycline also led to decreased cell death. Thus, anti-inflammatory treatments appear to be directly protective of neurons from in vitro ischemia.