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NMDA 预处理中的细胞信号转导与喹啉酸诱导惊厥中的神经保护作用。

Cell signaling in NMDA preconditioning and neuroprotection in convulsions induced by quinolinic acid.

机构信息

Centro de Biologia Molecular e Estrutural Departamento de Bioquímica CCB, Universidade Federal de Santa Catarina, Florianopolis, SC, Brazil.

出版信息

Life Sci. 2011 Oct 10;89(15-16):570-6. doi: 10.1016/j.lfs.2011.05.014. Epub 2011 Jun 13.

Abstract

The search for novel, less invasive therapeutic strategies to treat neurodegenerative diseases has stimulated scientists to investigate the mechanisms involved in preconditioning. Preconditioning has been report to occur in many organs and tissues. In the brain, the modulation of glutamatergic transmission is an important and promising target to the use of effective neuroprotective agents. The glutamatergic excitotoxicity is a factor common to neurodegenerative diseases and acute events such as cerebral ischemia, traumatic brain injury and epilepsy. In this review we focus on the neuroprotection and preconditioning by chemical agents. Specially, chemical preconditioning models using N-methyl-d-aspartate (NMDA) pre-treatment, which has demonstrated to lead to neuroprotection against seizures and damage to neuronal tissue induced by quinolinic acid (QA). Here we attempted to gather important results obtained in the study of cellular and molecular mechanisms involved in NMDA preconditioning and neuroprotection.

摘要

寻找新的、微创的治疗策略来治疗神经退行性疾病,这促使科学家们研究预处理所涉及的机制。预处理已被报道发生在许多器官和组织中。在大脑中,调节谷氨酸能传递是使用有效神经保护剂的一个重要且有前途的靶点。谷氨酸兴奋性毒性是神经退行性疾病和急性事件(如脑缺血、创伤性脑损伤和癫痫)的共同因素。在这篇综述中,我们重点关注化学药物的神经保护和预处理。特别是,使用 N-甲基-D-天冬氨酸(NMDA)预处理的化学预处理模型已被证明可以防止喹啉酸(QA)引起的癫痫发作和神经元组织损伤,从而起到神经保护作用。在这里,我们试图收集 NMDA 预处理和神经保护中涉及的细胞和分子机制的重要研究结果。

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