Testosterone enhances functional recovery after stroke through promotion of antioxidant defenses, BDNF levels and neurogenesis in male rats.

Abstract It is reported that circulating testosterone levels decrease after cerebral ischemia. The aim of this study was to evaluate the effects of testosterone on oxidative stress, brain-derived neurotrophic factor (BDNF) levels, neurogenesis, histological damage and sensorimotor recovery in a castrated male rat model of focal cerebral ischemia. Animals were divided into four groups. For all animals, castrations were conducted 7 days before transient middle cerebral artery occlusion (MCAO) was done and cerebral ischemia was induced. The first group served as sham. Second was MCAO group and received vehicle only, third was MCAO group that was post-treated with testosterone and the fourth was MCAO group post-treated with testosterone and flutamide. Treatment only with testosterone significantly weakened oxidative stress and increased BDNF levels and sensorimotor recovery during a 10 days period. Rats receiving testosterone demonstrated a significant reduction in infarct volume and a significant increase in neurogenesis on 10th day after focal cerebral ischemia. Our results for the first time showed a potential advantageous effect of testosterone after cerebral ischemia in male rats, which was probably mediated by promoting antioxidant defenses, BDNF levels and neurogenesis.