Edaravone and cyclosporine A as neuroprotective agents for acute ischemic stroke

作者：Shohei Matsumoto, Michihiro Murozono, Masahiro Kanazawa, Takeshi Nara, Takuro Ozawa, Yasuo Watanabe · 发表于：Acute Medicine & Surgery · 年份：2018 · DOI：10.1002/ams2.343 · 被引用次数：82 · 研究领域：Mitochondrial Function and Pathology、Neuroinflammation and Neurodegeneration Mechanisms、Adenosine and Purinergic Signaling

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.