Dihydromyricetin ameliorates oxygen‑glucose deprivation and re‑oxygenation‑induced injury in HT22 cells by activating the Wnt/β‑catenin signaling pathway.

Abstract

Dihydromyricetin (DMY) is a natural flavonoid that possesses a wide range of pharmacological properties. The aim of the present study was to determine whether DMY could protect against nerve cell injury following ischemic stroke through antioxidant and neuroprotective effects. The effects of DMY on the viability, oxidative stress and apoptosis of HT22 cells following oxygen-glucose deprivation and re-oxygenation (OGD/R) were examined using MTT, lactate dehydrogenase (LDH), superoxide (SOD), malondialdehyde (MDA), western blot and TUNEL assays. Furthermore, Wnt/β-catenin signaling proteins in OGD/R-stimulated HT22 cells were detected in the presence or absence of DMY. In a separate experiment, the effect of DMY on OGD/R-induced HT22 cell injury was also observed in the presence of the Wnt/β-catenin inhibitor, XAV939. The results demonstrated that DMY had no impact on the survival of untreated HT22 cells, although DMY treatment significantly increased cell viability and inhibited cytotoxicity, oxidative stress and apoptosis following OGD/R. In addition, DMY upregulated the expression of Wnt/β-catenin in OGD/R-stimulated HT22 cells. In conclusion, DMY protected HT22 cells from OGD/R-induced oxidative stress and apoptosis, and its effects may be mediated by the activation of the Wnt/β-catenin signaling pathway.