Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

Cerebral ischemia‑reperfusion injury (CIRI) refers to the phenomenon that ischemic of brain leads cells, which is further aggravated after recovery blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used HT22 hippocampal neurons mice, by sugar deprivation. DHM found increase viability cells following OGD/R induction. levels malondialdehyde (MDA) decreased, superoxide dismutase (SOD) glutathione (GSH) OGD/R‑induced increased treatment, accompanied decreased protein expression NOX2 NOX4. also inhibited apoptosis induced OGD/R, Bax caspase‑3, Bcl‑2. Moreover, NF‑E2‑related factor 2 (Nrf2)/heme oxygenase (HO‑1) signaling pathway‑associated proteins were oxidative stress reversed addition Nrf2/HO‑1 pathway inhibitor, brusatol. In conclusion, activating pathway.