Dihydromyricetin inhibits injury caused by ischemic stroke through the lncRNA SNHG17/miR-452-3p/CXCR4 axis.

ABSTRACT: Ischemic stroke (IS) is an important cause of death worldwide. Dihydromyricetin (DHM) has been reported to have neuroprotective potential, but its role and mechanism in IS have not been fully elucidated. The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was used to determine the safe dose of DHM in BV2 microglia and its applicability in OGD/R-treated cells. The mechanism of action of DHM was explored by RT-qPCR, ELISA, luciferase reporter gene assay and western blotting. DHM dose-dependently enhanced BV2 cell viability post-OGD/R and attenuated inflammation and oxidative stress. The protective effects of DHM were found to be mediated through the downregulation of SNHG17, which in turn modulated miR-452-3p expression. miR-452-3p was identified as a negative regula

SUBMITTER: Xie J 

PROVIDER: S-EPMC11786715 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature