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

Abstract

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 invivo 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 erythroid2‑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 invitro 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.