文献类型：期刊文献

英文题名：Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation-induced HT22 cells by activating the Nrf2/HO-1 pathway

作者：Zhang, Qian[1];Wang, Jia[2];Zhang, Huili[3];Zeng, Tao[3]

第一作者：Zhang, Qian

通信作者：Zeng, T[1]

机构：[1]Gansu Prov Hosp TCM, Dept Encephalopathy, Lanzhou 730050, Gansu, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Dept Rheumat Osteopathy, Affiliated Hosp, Lanzhou 730000, Gansu, Peoples R China;[3]South China Univ Technol, Guangzhou Peoples Hosp 1, Sch Med, Dept Neurol, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China

第一机构：Gansu Prov Hosp TCM, Dept Encephalopathy, Lanzhou 730050, Gansu, Peoples R China

通信机构：[1]corresponding author), South China Univ Technol, Guangzhou Peoples Hosp 1, Sch Med, Dept Neurol, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China.

年份：2021

卷号：23

期号：6

外文期刊名：MOLECULAR MEDICINE REPORTS

收录：;Scopus(收录号：2-s2.0-85103683004);WOS:【SCI-EXPANDED(收录号:WOS:000639212100001)】；

基金：The present study was supported by The Science Foundation of Guangzhou First People's Hospital (grant no. M2019022).

语种：英文

外文关键词：dihydromyricetin; cerebral ischemia reperfusion injury; oxidative stress; apoptosis; oxygen and glucose deprivation; reoxygenation; Nrf2; HO-1 pathway

摘要：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 HT22 cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R-induced HT22 cells 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 factor 2 (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 HT22 cells by activating the Nrf2/HO-1 signaling pathway.