miR-495-3p attenuates cerebral ischemia-reperfusion-induced neuronal inflammation and apoptosis by targeting CCL2 expression.

This study aimed to explore the function of miR-495-3p in cerebral ischemia-reperfusion injury (CI/RI) and reveal its potential molecular mechanism. In vivo and in vitro models of CI/RI were established by MACO/R and OGD/R, respectively. Neural function scores, HE staining, and TUNEL staining assessed the degree of brain tissue injury in mice. LDH assay, MTT assay, and flow cytometry evaluated neuronal toxicity, viability, and apoptosis rate. ELISA and Western blot evaluated inflammatory factors and the NF-κB pathway. Dual-luciferase reporting assay and RIP explored the targeting relationship between miR-495-3p and CCL2. miR-495-3p was abnormally low in MACO/R mouse brain tissue and OGD/R-damaged neurons, while CCL2 was highly expressed. miR-495-3p overexpression improved neuronal apoptosis and inflammation in the brain tissue of MACO/R mice. Consistent results were also obtained in in vitro experiments. Enhancing CCL2 or knocking down miR-495-3p aggravated OGD/R-induced neuronal damage. The deleterious effects of miR-495-3p knockdown were prevented by the knockdown of CCL2. miR-495-3p targeted CCL2. miR-495-3p improves CI/R-mediated neuronal apoptosis and inflammation through targeted regulation of CCL2 expression. These results provide data support for CI/RI-targeting drugs and the understanding of disease mechanisms.