Nucci Carlo, Tartaglione Rosanna, Cerulli Angelica, Mancino R, Spanò A, Cavaliere Federica, Rombolà Laura, Bagetta G, Corasaniti M Tiziana, Morrone Luigi A
Physiopathological Optics, Department of Biopathology, University of Rome Tor Vergata 00133 Rome, Italy.
Int Rev Neurobiol. 2007;82:397-406. doi: 10.1016/S0074-7742(07)82022-8.
Recent studies support a role for excitotoxicity in the development of retinal ganglion cell (RGC) damage in subjects suffering from glaucoma. Coenzyme Q10 (CoQ10), an essential cofactor of the electron transport chain, has been reported to afford neuroprotection, preventing the formation of the mitochondrial permeability transition pore. Using an established animal model of retinal ischemia/reperfusion here, we show that synaptic glutamate increases at 130min from beginning of reperfusion and delayed apoptosis in the RGC layer is seen at 24h. Intraocular administration of CoQ10 minimizes glutamate increase and affords neuroprotection, suggesting that oxidative stress and energy failure might be implicated in the mechanisms of RGC death.
最近的研究支持兴奋性毒性在青光眼患者视网膜神经节细胞（RGC）损伤发展中的作用。辅酶Q10（CoQ10）是电子传递链的一种必需辅助因子，据报道具有神经保护作用，可防止线粒体通透性转换孔的形成。在此，我们使用已建立的视网膜缺血/再灌注动物模型，发现再灌注开始130分钟时突触谷氨酸增加，24小时时在RGC层可见延迟性细胞凋亡。眼内给予CoQ10可使谷氨酸增加最小化并提供神经保护，这表明氧化应激和能量衰竭可能与RGC死亡机制有关。
