Isoquercetin activates the ERK1/2-Nrf2 pathway and protects against cerebral ischemia-reperfusion injury in vivo and in vitro
- Miao Chen
- Li‑Hua Dai
- Aihua Fei
- Shu‑Ming Pan
- Hai‑Rong Wang
Affiliations: Department of Emergency, Xinhua Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200092, P.R. China
- Published online on: January 31, 2017 https://doi.org/10.3892/etm.2017.4093
Copyright: © Chen
et al. This is an open access article distributed under the
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Isoquercetin has exhibited a wide range of therapeutic properties, including antioxidant, anti-inflammatory and anti‑allergic activities. The aim of the present study was to investigate the effect of isoquercetin on rats with 2 h middle cerebral artery occlusion (MCAO) and evaluate the neuroprotective effect of isoquercetin on a primary culture of rat hippocampal neuronal cells subjected to oxygen‑glucose deprivation followed by reoxygenation (OGD/R). In vivo, the rats treated with isoquercetin exhibited a lower degree of neurological dysfunction and smaller infarct volume than the vehicle‑treated rats. In vitro, it was found that isoquercetin prevented the OGD/R‑induced increase in apoptosis, lactate dehydrogenase release and reduction in cell viability. Additionally, isoquercetin induced the upregulation of nuclear factor erythroid 2-related factor 2 gene and protein expression, and increased extracellular signal‑regulated kinase 1 and 2 (ERK1/2) phosphorylation. This indicates that the ERK1/2 pathway may contribute to the neuroprotective effect of isoquercetin against OGD/R‑induced oxidative damage in rat hippocampal neurons. These findings suggest the potential importance of isoquercetin in the treatment of ischemia/reperfusion-related brain injury and associated diseases.