Sirt1/Nrf2 signalling pathway prevents cognitive impairment in diabetic rats through anti-oxidative stress induced by miRNA-23b-3p expression

In the present study the exact roles and mechanisms underlying the effect of miRNA-23b-3p on the cognitive impairment of diabetic rats were investigated. The in vivo model of diabetes was established in Wistar rats via a single injection of streptozotocin (STZ). Cognitive function was evaluated using a Morris water maze test. Oxidative stress was measured using ELISA kits, and the protein expression levels of B-cell lymphoma 2-associated X protein, silent information regulator 1 (SIRT1), nuclear factor erythroid 2-related factor 2 (Nrf2) and GAPDH were measured by western blot analysis. Micro (mi)RNA-23b-3p mimics were employed to increase miRNA-23b-3p expression in the in vitro model. Overexpression of miRNA-23b-3p increased oxidative stress (as indicated by the levels of glutathione peroxidase, glutathione, superoxide dismutase and malondialdehyde) and apoptosis in neurocytes following high-glucose treatment. The overexpression of miRNA-23b-3p also suppressed SIRT1 and Nrf2 expression in neurocytes following high-glucose treatment; it also promoted the SIRT1-induced inhibition of apoptosis and oxidative stress. The promotion of SIRT1 also decreased the effect of miRNA-23b-3p on cognitive impairment in diabetic rats. In conclusion, miRNA-23b-3p prevents the cognitive impairment of diabetic rats via anti-oxidative stress effects and the Sirt1/Nrf2 signaling pathway.