期刊
BRAIN RESEARCH
卷 1750, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.brainres.2020.147165
关键词
Oxygen-glucose deprivation/reoxygenation; Keap1; Neuron; Nrf2; Sesn1
The study demonstrates that Sesn1 exerts neuroprotective effects on neurons following cerebral ischemia/reperfusion injury by potentiating Nrf2 activation to ameliorate OGD/R-induced damage.
Sestrin1 (Sesn1) acts as a stress-inducible protein that performs a remarkable cytoprotective function upon diverse cellular stresses. However, whether Sesn1 exerts a cytoprotective role in neurons following cerebral ischemia/reperfusion injury is unknown. The goal of this work was to evaluate the role of Sesn1 in oxygen glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury in vitro. The induction of Sesn1 was found in neurons exposed to OGD/R treatment. The silencing of Sesn1 rendered neurons more vulnerable to OGD/R injury, while the up-regulation of Sesn1 ameliorated OGD/R-induced neuronal injury by reducing apoptosis and the generation of reactive oxygen species (ROS). Furthermore, the up-regulation of Sesn1 promoted the activity of the nuclear factor-erythroid 2-related factor 2 (Nrf2) by down-regulating the expression of the Kelchlike ECHassociated protein 1 (Keap1). The restoration of Keap1 or the suppression of Nrf2 remarkably abolished the Sesn1-induced neuroprotection effects in OGD/R-exposed neurons. In summary, our work indicates that Sesn1 is a remarkable neuroprotective protein that potentiates Nrf2 activation via Keap1 to ameliorate OGD/R-induced injury.
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