Abstract Objectives Ischemic stroke is a major global cause of mortality and long-term disability, resulting in irreversible neuronal damage, cognitive impairment, and reduced quality of life. To investigate the neuroprotective role of miR-134-3p in ischemic stroke and elucidate its regulatory mechanism targeting MMP-8. Methods The middle cerebral artery occlusion (MCAO) model was established in mice to simulate ischemic stroke injury. Neuronal cell models subjected to oxygen-glucose deprivation (OGD) simulated ischemic conditions in vitro . The modified neurological severity score (mNSS), inflammation marker assays, cell viability tests, and luciferase reporter assays assessed functional outcomes and molecular interactions. Results MiR-134-3p expression was downregulated following ischemic injury both in vivo and in vitro . Overexpression of miR-134-3p improved neuronal survival, reduced inflammatory cytokine levels, and mitigated neurological deficits. Mechanistic studies demonstrated that miR-134-3p negatively regulated MMP-8 expression by binding its 3′ UTR directly. Furthermore, miR-134-3p overexpression reversed the detrimental effects induced by MMP-8 upregulation on neuronal viability. Conclusions MiR-134-3p showed a protective effect against ischemic stroke-induced neural damage through targeted suppression of MMP-8. And the therapeutic potential for targeting the miR-134-3p/MMP-8 axis as an intervention strategy for ischemic brain injury.
Yu et al. (Sat,) studied this question.