H2O2 - mediated SRPED1 Inactivation Contributes to Resisting Ischemia-reperfusion Induced Oxidative Injury to Microglia

Abstract Oxidative stress induced by ischemia-reperfusion is an important reason for the loss of neurons in the brain. In addition to direct oxidative toxicity that causes apoptosis of neurons and glial cells, oxidative stress can also cause complex physiological effects of related cells, such as activation of microglia to promote their repair effects on damaged areas. Here, we found that SPRED1, sprouty-related protein with an EVH1 domain 1, was significantly inhibited after ischemia-reperfusion by MCAO in rats, while the inhibition of SPRED1 responded to the up-expressed p65 proteins with the stimulation of H 2 O 2 . What’s more, we further revealed that SPRED1 tended to exert a unique role in maintaining intracellular homeostasis, which can re-activate the instinct of microglia upon the induction of H 2 O 2 to resist oxidative toxicity. However, SPRED1 did not show such ability when it is only over-expressed but without H 2 O 2 induction. In a word, these data revealed a potential role of SPRED1 in preventing cerebral ischemia-induced oxidative stress injury to nerve cells.