Abstract
BACKGROUND: We explore the effect of improving cognitive dysfunction after cerebral ischemia-reperfusion (CI/R) by regulating HCG27. METHODS: The MCAO and OGD/R methods were employed to establish in vivo and in vitro models of cognitive dysfunction caused by a CI/R injury. RT-qPCR was utilized to detect the relative expression of HCG27 and miR-27a-3p. An ELISA was adopted to measure the concentrations of inflammatory factors (IL-6, IL-1β, IL-10). The concentration of MDA and activity of CAT were detected using commercially available kits. The neurological deficit was evaluated using the mNSS score. The spatial learning and memory capabilities were evaluated via the MWM test. The targeting relationships were validated by the dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. The CCK-8 assay and flow cytometry were employed to asses cell viability and apoptosis, respectively. RESULTS: The level of HCG27 was upregulated in MCAO rats and OGD/R-induced BV2 cells, whereas that of miR-27a-3p decreased, and HCG27 targeted miR-27a-3p. Compared with the sham group, the mNSS score of MCAO rats was elevated, and their spatial learning and memory abilities declined, with aggravated inflammatory response and oxidative stress. However, silencing HCG27 improved these conditions, and the miR-27a-3p antagonist reversed this. MiR-27a-3p reversed the increase in cell viability in OGD/R-induced BV2 cells, reduced the cell apoptosis rate, and weakened the inflammatory response and oxidative stress caused by the HCG27 silencing. CONCLUSIONS: Silencing HCG27 can protect against cognitive dysfunction after cerebrovascular disease by targeting miR-27a-3p.