脑缺血的损伤机制及其保护性干预(英文)

• 作 者: 郭朝晖 李峰 王维治
• 机 构: 哈尔滨医科大学第二附属医院神经科,
• 出 处: Neuroscience Bulletin
• 发表日期: 2009年03期
• 关键词: 脑保护治疗 脑缺血 谷氨酸受体 钙毒性 谷氨酸兴奋毒性 内质网应激 内质网 前适应 级联反应 钙通道

脑缺血的损伤机制包括谷氨酸兴奋毒性、钙毒性、自由基、一氧化氮、炎性反应以及内质网和线粒体功能障碍等。这些损伤性级联反应相互联系,错综复杂,很难比较它们在不同模型中的主次作用。越来越多的对细胞及分子损伤途径的基础研究,推动了对脑保护治疗的研究。迄今为止,脑保护治疗仍以药物治疗为主,例如,抗兴奋毒性治疗、钙通道阻滞、抗氧化、抗炎、抗凋亡治疗等。此外一些研究还包括溶栓、动脉生成和神经元再生,以及缺血前适应和缺血后适应等。虽然将这些研究成果应用于临床还存在许多困难,但是通过改进动物实验和临床实验方法,我们有理由对脑保护治疗持乐观的态度。

Damage mechanisms of cerebral ischemia include glutamate excitotoxicity, calcium toxicity, free radicals, nitric oxide, inflammatory response and endoplasmic reticulum and mitochondrial dysfunction. These damaging cascades are interconnected and intricate and difficult to compare their primary and secondary roles in different models. More and more basic research on the pathways of cell and molecular damage has promoted the study of brain protection therapy. To date, brain protection is still dominated by medical treatments such as anti-excitotoxic therapy, calcium channel blockade, anti-oxidant, anti-inflammatory and anti-apoptotic therapies. In addition, some studies include thrombolysis, arterial generation and neuronal regeneration, and pre-ischemic adaptation and post-ischemic adaptation. Although there are many difficulties in applying these findings to clinical practice, we can reasonably be optimistic about brain protection by improving animal experiments and clinical trials.