Quercetin attenuates the injury-induced reduction of γ-enolase expression in a middle cerebral artery occlusion animal model.

Quercetin, a natural flavonoid, copiously exists in vegetable, fruits and tea. Quercetin is beneficial to neurodegenerative disorders via its strong anti-oxidant and anti-inflammatory activities. γ-Enolase is one of the enzymes of glycolytic pathway and is predominantly expressed in neuronal cells. The aim of the present study is to verify whether quercetin modulates the expression of γ-enolase in brain ischemic injury. Adult Sprague-Dawley male rats were subjected to middle cerebral artery occlusion (MCAO) and quercetin (50 mg/kg) or vehicle was administered by intraperitoneal injection at 1 h before MCAO onset. A proteomics study, Western blot analysis, reversetranscription-PCR, and immunofluorescence staining were conducted to investigate the change of γ-enolase expression level. We identified a decline in γ-enolase expression in MCAO-operated animal model using a proteomic approach. However, quercetin treatment significantly attenuated this decline. These results were confirmed using Western blot analysis, reverse transcription-PCR, and immunofluorescence staining techniques. γ-Enolase is accepted as a neuron specific energy synthesis enzyme, and quercetin modulates γ-enolase in a MCAO animal model. Thus, our findings can suggest the possibility that quercetin regulates γ-enolase expression in response to cerebral ischemia, which likely contributes to the neuroprotective effect of quercetin.