Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22cells by activating the Nrf2/HO‑1 pathway.

Abstract

Cerebral ischemia‑reperfusion injury (CIRI) refers to the phenomenon that ischemic injury of the brain leads to the injury of brain cells, which is further aggravated after the recovery of blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI has not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used on HT22 hippocampal neurons in mice, by oxygen and sugar deprivation. DHM was found to increase the cell viability of HT22cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R‑induced HT22cells increased following DHM treatment, accompanied by the decreased protein expression levels of NOX2 and NOX4. DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2. Moreover, the expression levels of the NF‑E2‑related factor2 (Nrf2)/heme oxygenase (HO‑1) signaling pathway‑associated proteins in OGD/R‑induced HT22 were increased following DHM treatment, and the effect of DHM on oxidative stress and apoptosis was reversed after the addition of the Nrf2/HO‑1 pathway inhibitor, brusatol. In conclusion, DHM inhibited oxidative stress and apoptosis in OGD/R‑induced HT22cells by activating the Nrf2/HO‑1 signaling pathway.