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Dihydromyricetin inhibits injury caused by ischemic stroke through the lncRNA SNHG17/miR-452-3p/CXCR4 axis
Jiacheng Xie1, Qiuyue Yang1, Xueliang Zeng2
1Department of Pathology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
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 regulator of pro-inflammatory CXCR4, a direct target whose expression was inversely affected by SNHG17. The interaction between SNHG17 and miR-452-3p was further confirmed by RNA pull-down assays. Furthermore, manipulation of the SNHG17/miR-452-3p/CXCR4 axis was shown to modulate the NF-κB signaling pathway as evidenced by changes in phosphorylation levels. In conclusion, our findings elucidate a novel DHM-mediated neuroprotective mechanism in microglial cells involving the SNHG17/miR-452-3p/CXCR4 regulatory axis. This axis attenuates OGD/R-induced inflammatory and oxidative stress, suggesting a therapeutic potential for DHM in conditions characterized by such pathological processes.
Insights
Dihydromyricetin (DHM) protects brain cells from ischemic stroke damage by reducing inflammation and oxidative stress. It works by regulating the SNHG17/miR-452-3p/CXCR4 pathway in microglial cells, offering therapeutic potential.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Ischemic stroke (IS) is a leading global cause of mortality.
- Dihydromyricetin (DHM) shows potential neuroprotection, but its mechanism in IS requires clarification.
- Microglial cells play a critical role in neuroinflammation and oxidative stress during IS.
Purpose of the Study:
- To investigate the neuroprotective role and underlying mechanism of DHM in an in vitro model of ischemic stroke.
- To elucidate the specific molecular pathways modulated by DHM in microglial cells.
Main Methods:
- MTT assay to determine DHM safety and efficacy in OGD/R-treated BV2 microglia.
- RT-qPCR, ELISA, luciferase reporter gene assay, and western blotting to explore DHM's mechanism.
- RNA pull-down assays to confirm molecular interactions.
Main Results:
- DHM dose-dependently increased BV2 cell viability and reduced inflammation and oxidative stress post-OGD/R.
- DHM downregulated SNHG17, which modulated miR-452-3p expression.
- miR-452-3p negatively regulated CXCR4, with SNHG17 inversely affecting CXCR4 expression.
- The SNHG17/miR-452-3p/CXCR4 axis modulated the NF-κB signaling pathway.
Conclusions:
- DHM exerts neuroprotection in microglial cells via the SNHG17/miR-452-3p/CXCR4 axis.
- This pathway attenuates OGD/R-induced inflammatory and oxidative stress.
- DHM demonstrates therapeutic potential for conditions involving microglial-mediated inflammation and oxidative stress.
