![]() ![]() This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper and its Supporting Information files.įunding: This work was supported by the National Natural Science Foundation of China (31960177 to LJ), the Key Research and Development Program of Ningxia (2021BEG03076 to YMM), the Natural Science Foundation of Ningxia (2021AAC03152 to YMM). ![]() Received: JAccepted: AugPublished: September 8, 2023Ĭopyright: © 2023 Li et al. (2023) Selenium inhibits ferroptosis in hyperglycemic cerebral ischemia/reperfusion injury by stimulating the Hippo pathway. The findings suggest that pretreatment with sodium selenite can regulate ferroptosis by activating the Hippo pathway, and minimize hyperglycemia-mediated exacerbation of cerebral I/R injury.Ĭitation: Li L, Wang M, Ma Y-M, Yang L, Zhang D-H, Guo F-Y, et al. The Hippo pathway inhibitor XMU-MP-1 eliminated the inhibitory effect of sodium selenite on ferroptosis. Furthermore, we observed that pretreatment with sodium selenite increased YAP and TAZ levels in the cytoplasm while decreasing YAP and TAZ levels in the nucleus. Pretreatment with sodium selenite reduced the hyperglycemia mediated enhancement of ferroptosis. Moreover, sodium selenite pretreatment increased the survival rate of HT22 cells under OGD/R and high glucose conditions. The results showed that hyperglycemia exacerbated cerebral I/R injury, and sodium selenite pretreatment decreased infarct volume, edema and neuronal damage in the cortical penumbra. An in vitro model of hyperglycemic cerebral I/R injury was created with oxygen-glucose deprivation and reoxygenation (OGD/R) and high glucose was employed. Middle cerebral artery occlusion (MCAO) and reperfusion models were established in rats under hyperglycemic conditions. The aim of this study was to examine how selenium alleviates hyperglycemia-mediated exacerbation of cerebral I/R injury by regulating ferroptosis. Our previous research showed that selenium (Se) could alleviate this injury. Hyperglycemia can exacerbate cerebral ischemia/reperfusion (I/R) injury, and the mechanism involves oxidative stress, apoptosis, autophagy and mitochondrial function. ![]()
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