Abstract: Objective To explore the mechanism by which LncRNA SNHG8 regulates miR-494-3p expression to alleviate cerebral ischemia-reperfusion injury. Methods A mouse model of cerebral ischemia-reperfusion injury was established, and TTC staining was used to determine the infarct area; ELISA was used to detect the contents of the inflammatory factors IL-1β, IL-6 and TNF-α in the brain tissue, and RT-qPCR was performed to detect the expression levels of LncRNA MALAT1 and miR-155- 5p. A microglial cell model overexpressing LncRNA SNHG8 was exposed to oxygen-glucose deprivation/reoxygenation (OGD/R), and inflammatory reaction and apoptosis of the cells were detected using ELISA and flow cytometry. A luciferase reporter assay was used to detect the targeting relationship between LncRNA SNHG8 and miR-494-3p. We further constructed a microglial cell model overexpressing both LncRNA SNHG8 the miR-494-3p, and examined inflammatory reactions and apoptosis of the cells following OGD/R exposure. Results In the mouse model of cerebral ischemia-reperfusion injury, the contents of inflammatory factors IL-1β, IL-6 and TNF-α increased significantly in the brain tissue (P<0.001), where LncRNA SNHG8 expression was lowered (P<0.01) and miR-494-3p expression increased significantly (P<0.01). In the microglial cells, overexpression of LncRNA SNHG8 significantly inhibited the inflammatory reaction and apoptosis following OGD/R exposure (P<0.01), and overexpression of LncRNA SNHG8 strongly inhibited the expression of miR-494-3p (P<0.01). Overexpression of miR-494-3p in microglia overexpressing SNHG8 partially promoted inflammatory reaction and cell apoptosis in response to OGD/R (P<0.05). Conclusion LncRNA SNHG8 can improve cerebral ischemia-reperfusion injury in mice by inhibiting the expression of miR-494-3p and suppressing inflammatory reactions and apoptosis of the microglia.

Key words: cerebral ischemia-reperfusion injury; LncRNA SNHG8; miR-494-3p; inflammatory reaction; apoptosis