LINC01128 alleviates neuronal injury and neurological deficits after ischemic stroke via targeting miR-92a-3p

Ischemic stroke is a severe cerebrovascular disease. Focusing on ischemic stroke, this study aims to determine LINC01128 expression changes and its mechanism involving miR-92a-3p regulation.

A rat model of middle cerebral artery occlusion and an oxygen-glucose deprivation/reoxygenation model of SH-SY5Y cells were established to simulate ischemic stroke. Reverse transcription-quantitative polymerase chain reaction was used to detect the expression of LINC01128 and miR-92a-3p. Dual luciferase reporter gene, RNA immunoprecipitation, and RNA pull-down experiments were used to verify the molecular interactions. ELISA and reactive oxygen species (ROS) assays were used to evaluate the levels of inflammation and oxidative stress. The neurological function was evaluated by foot fault test, corner test, and modified neurological severity score.

LINC01128 expression was markedly decreased, whereas miR-92a-3p expression was increased in ischemic stroke models. Experiments confirmed that LINC01128 directly binds to miR-92a-3p. In-vivo models demonstrated that LINC01128 overexpression effectively reduced proinflammatory factor levels and ROS production, increased the anti-inflammatory factor, and improved neurological dysfunction. Overexpression of LINC01128 also mitigated oxygen-glucose deprivation/reoxygenation-induced apoptosis, inflammation, and intracellular ROS accumulation while enhancing cell viability. However, all these protective effects were reversed by co-overexpression of miR-92a-3p.

LINC01128 exerts a crucial neuroprotective effect in ischemic stroke models by targeting miR-92a-3p, effectively alleviating neuroinflammation and oxidative stress damage while improving neurological deficits. The discovery of the LINC01128/miR-92a-3p regulatory axis provides new insights into the molecular mechanisms underlying poststroke neural injury.