Study on the Mechanism of miR-124-3p Regulating Cerebral Ischemia-Reperfusion Injury

Abstract

Objective: To investigate the role of miR-124-3p in ischemia-reperfusion injury following ischemic stroke and to evaluate the neuroprotective effects of miR-124-3p inhibition on neurological outcomes, infarct size, and apoptosis. Methods: A middle cerebral artery occlusion (MCAO) model was used to induce ischemia-reperfusion injury in rats. Experimental groups included a sham surgery group, an MCAO group, an MCAO + miR-124-3p NC group, and an MCAO + miR-124-3p antagomir group. Neurological deficits were assessed at 2, 8, and 24 hours post-ischemia. Infarct size and apoptosis levels were measured using brain tissue weight analysis and TUNEL assay, respectively, to evaluate the extent of ischemic damage and cell death. Results: The MCAO group showed progressively worsening neurological deficits, increased infarct size, and extensive apoptosis. In contrast, miR-124-3p inhibition significantly reduced neurological deficits, with lower scores at all time points. The MCAO + miR-124-3p inhibitor group demonstrated a significant reduction in infarct size compared to the MCAO group and the NC group, suggesting tissue preservation. Additionally, the miR-124-3p inhibitor group showed markedly reduced apoptosis, as evidenced by decreased TUNEL-positive signals, indicating a reduction in cell death following ischemia-reperfusion injury. Conclusion: Inhibition of miR-124-3p plays a neuroprotective role in ischemia-reperfusion injury by mitigating neurological deficits, reducing infarct size, and lowering apoptosis levels. These findings suggest that miR-124-3p inhibition could be a promising therapeutic target for minimizing brain damage and improving recovery in ischemic stroke patients.