Matsumoto Shohei, Murozono Michihiro, Kanazawa Masahiro, Nara Takeshi, Ozawa Takuro, Watanabe Yasuo
Department of Anesthesiology SUBARU Health Insurance Association Ota Memorial Hospital Gunma Japan.
Department of Anesthesiology Tokyo Medical University Ibaraki Medical Center Ibaraki Japan.
Acute Med Surg. 2018 May 17;5(3):213-221. doi: 10.1002/ams2.343. eCollection 2018 Jul.
It is well known that acute ischemic stroke (AIS) and subsequent reperfusion produce lethal levels of reactive oxygen species (ROS) in neuronal cells, which are generated in mitochondria. Mitochondrial ROS production is a self-amplifying process, termed "ROS-induced ROS release". Furthermore, the mitochondrial permeability transition pore (MPTP) is deeply involved in this process, and its opening could cause cell death. Edaravone, a free radical scavenger, is the only neuroprotective agent for AIS used in Japan. It captures and reduces excessive ROS, preventing brain damage. Cyclosporine A (CsA), an immunosuppressive agent, is a potential neuroprotective agent for AIS. It has been investigated that CsA prevents cellular death by suppressing MPTP opening. In this report, we will outline the actions of edaravone and CsA as neuroprotective agents in AIS, focusing on their relationship with ROS and MPTP.
众所周知，急性缺血性中风（AIS）及随后的再灌注会在神经元细胞中产生致死水平的活性氧（ROS），这些ROS在线粒体中生成。线粒体ROS生成是一个自我放大的过程，称为“ROS诱导的ROS释放”。此外，线粒体通透性转换孔（MPTP）深度参与此过程，其开放可导致细胞死亡。依达拉奉是一种自由基清除剂，是日本唯一用于AIS的神经保护剂。它捕获并减少过量的ROS，预防脑损伤。环孢素A（CsA）是一种免疫抑制剂，是AIS潜在的神经保护剂。已有研究表明，CsA通过抑制MPTP开放来防止细胞死亡。在本报告中，我们将概述依达拉奉和CsA作为AIS神经保护剂的作用，重点关注它们与ROS和MPTP的关系。
