17β-Estradiol Attenuates a Reduction of Gamma-Enolase Following Cerebral Ischemic Injury

Abstract

Neuron-specific enolase (NSE), a glycolytic enzyme specifically expressed in neurons, enhances thesurvival of neurons and exerts neuroprotective effects. Previous study has been shown that estradiolexerts neuroprotective effects against neuronal cell injury. This study investigated whether 17β-estradiolregulates NSE expression in middle cerebral artery occlusion (MCAO)-induced injury and glutamateexposure-induced neuronal cell death. Adult female rats were ovariectomized and treated with oil or 17β-estradiol prior to MCAO. Brains were collected at 24 hr after MCAO and the cerebral cortices wereisolated. Using a proteomics technique, NSE protein spots are differentially expressed in oil- and 17β-estradiol-treated rats. Western blot analysis demonstrated that ischemic injury induces a decrease in NES,pretreatment with 17β-estradiol prevents injury-induced decrease in NSE. Furthermore, glutamateexposure induced a decrease in NSE in a hippocampal-derived cell lines, and pretreatment with 17β-estradiol prevented the glutamate toxicity-induced decrease in NSE. The results of this study suggest that17β-estradiol mediates neuroprotective effects during neuronal cell damage by regulating the expressionof NSE.