Novel neuroprotectant lithium in thrombolytic therapy

为探讨锂联合组织型纤溶酶原激活剂（t-PA）溶栓治疗脑卒中的神经保护作用，本研究尝试建立临床相似的脑卒中动物模型。在尝试了几种实验条件后，我建立了在早期时间点给予t-PA显示血栓溶解和神经改善的模型，并且在晚期时间点给予t-PA也显示包括出血增加在内的恶化结局。由于技术上的困难，类似的动物模型在许多报道中没有使用。局灶性脑缺血后给予氯化锂通过细胞凋亡抑制神经退行性变。这种保护作用与Akt的激活无关。

To investigate the neuroprotective effect of lithium with tissue plasminogen activator(t-PA) in thrombolytic therapy in stroke, I tried to establish the clinically-resembling animal stroke model. After several experimental condition had been tried, I've established the model that showed thrombolysis and neurological improvement by t-PA administration in early time point, and also showed worsened outcome including increased hemorrhage by t-PA administration in late time point. Similar animal model is not used in many reports because of the technical difficulty. Administration of lithium chloride after focal brain ischemia suppressed neurodegeneration through apoptosis. This protective effect was not related the activation of Akt.