Inducing excitotoxicity, cerebral ischemia/reperfusion (I/R) injury Intracerebral hemorrhage or subarachnoid hemorrhage ( 1), is associated with high morbidity and
Neurological function caused by ischemia of the brain, Stroke, which is characterized by loss of In conclusion, MH combined with EDA exerted synergistic neuroprotective effects against cerebral I/R injury involving changes in the Nrf2/HO‑1 pathway. Western blotting demonstrated that the combined treatment with MH and EDA promoted the nuclear localization of Nrf2, and increased the levels of NAD(P)H quinone oxidoreductase and heme oxygenase (HO)‑1. The levels of glutathione (GSH), GSH peroxidase, catalase and superoxide dismutase in rat ischemic hemisphere tissues were reduced by Bru. However, MH in combination with EDA reversed the effects of MCAO, which were blocked by Bru injection. It was observed that mice treated by MCAO had higher neurological deficit scores and oxidative stress levels, and low spatial learning and memory capacity moreover, the CA1 region of the hippocampi of the mice exhibited reduced neuronal density and viability, and reduced mitochondrial dysfunction. A rat cerebral I/R injury model was constructed by middle cerebral artery occlusion (MCAO) followed by reperfusion, and the mice were treated by MH, EDA or the inhibitor of the Nrf2 signaling pathway brusatol (Bru). The aim of the present study was to investigate the effects and mechanism of action of MH in combination with EDA in cerebral I/R injury. However, whether MH and EDA exert synergistic effects against cerebral I/R injury remains unknown. Mild hypothermia (MH) and edaravone (EDA) exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury through activation of the nuclear factor erythroid 2‑related factor 2 (Nrf2) pathway.