Minoxidil Suppressed Mitochondrial Depolarization and Subsequent Neuronal Cell Death by Decreasing Intracellular Potassium Level

The study conducted six years ago investigated the effects of Minoxidil, a potassium channel opener, on neuronal tissue damage caused by transient focal cerebral ischemia. The experiment was performed on 6-week old male C57/BL6 mice, which were divided into four groups and treated with either saline, edaravone (6 mg/kg bw), or minoxidil (0.5 or 5 mg/kg bw) immediately after inducing ischemia. The results showed that transient focal cerebral ischemia decreased cellular respiration activity by 50% in the affected area, indicating neuronal tissue damage. However, immediate injection of edaravone or 5 mg/kg bw minoxidil significantly prevented this decrease. The study concluded that Minoxidil, originally developed for hypertension and now used for androgenic alopecia, could potentially be used to protect the central nervous system from damage due to its ability to open ATP-sensitive potassium channels.