Abstract

Curcumin can alleviate cerebral ischemia/reperfusion injury, but its mediated mechanism is still unclear. The study aimed to investigate whether curcumin mediates cerebral ischemia/reperfusion injury-impelled neuronal damage by microRNA-145-5p. An oxygen-glucose-deprivation/reperfusion model was conducted using rat hippocampal neuron HT22. Detection of catalase and superoxide dismutase activities and malondialdehyde content by a matching reagent kit was carried out to assess cellular oxidative stress. Interleukin-6, interleukin-10, and tumor necrosis factor-alpha were assessed for inflammation analysis. Relative microRNA-145-5p expression was detected by quantitative polymerase chain reaction. Oxygen-glucose-deprivation/reperfusion stimulation prompted the release of interleukin-10, interleukin-6, and tumor necrosis factor-alpha, lessened the activities of catalase and superoxide dismutase, as well as elevated the content of malondialdehyde in neurons HT22, but these alterations were undercut by curcumin in a concentration-dependent manner, suggesting that curcumin impaired oxygen-glucose-deprivation/reperfusion-prompted HT22 cell inflammation and oxidative stress. MicroRNA-145-5p silencing overtly reduced oxygen-glucose-deprivation/reperfusionprompted HT22 cell inflammation and oxidative stress. Curcumin treatment significantly decreased oxygenglucose- deprivation/reperfusion-mediated upregulation of microRNA-145-5p in neurons HT22. Moreover, in oxygen-glucose-deprivation/reperfusion-stimulated neurons HT22, the upregulation of microRNA-145-5p overexpression partly reversed cur-mediated changes regarding pro-inflammatory factors and indicators of oxidative stress. Curcumin could reduce microRNA-145-5p expression in oxygen-glucose-deprivation/ reperfusion-stimulated neurons, thus weakening neuronal inflammation and oxidative stress.