Novel neuroprotectant lithium in thrombolytic therapy

溶栓治疗中的新型神经保护剂锂

• 批准号: 22790813
• 负责人: TAKAHASHI Tetsuya
• 金额: $ 2.41万
• 依托单位: Niigata University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22790813/
• 关键词: 脳塞栓モデル; リチウム; 神経保護; Akt; 脳梗塞; 血栓溶解療法; 組織プラスミノゲンアクチベータ(t-PA)

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.

为了研究中风中溶栓疗法中锂与组织纤溶酶原激活剂（T-PA）的神经保护作用，我试图建立临床上令人发指的动物中风模型。在尝试了几个实验条件之后，我建立了该模型，该模型在早期时间点显示了T-PA给药的溶栓和神经系统改善，并且还显示出恶化的结果，包括在晚期T-PA给药的出血增加。由于技术困难，许多报告中没有使用类似的动物模型。局灶性脑缺血后氯化锂通过细胞凋亡抑制神经退行性。这种保护作用与AKT的激活无关。

项目成果

Lithium treatment reduces brain injury induced by focal ischemia with partial reperfusion and the protective mechanisms dispute the importance of akt activity.

• 发表时间: 2012-03
• 期刊: Aging and disease
• 影响因子: 7.4
• 作者: Tetsuya Takahashi;G. Steinberg;Heng Zhao