Electroacupuncture improves learning and memory deficits in diabetic encephalopathy rats by regulating the Nrf2/HO-1 pathway

[Display omitted] •Significant learning and memory deficits observed in DE rats.•EA boosts learning and memory capacity in DE rats.•Neurogenesis and morphological changes in the hippocampus following EA treatment.•Modulation of Nrf2/HO-1 pathway by EA mitigates behavioral and neuronal deficits. High blood sugar caused by diabetic encephalopathy(DE) can lead to excessive accumulation of reactive oxygen species in the brain, induce oxidative stress, and subsequently cause neuronal degeneration and apoptosis. The Nrf2/HO-1 signaling pathway is one of the most important pathways in oxidative stress response, but the precise mechanism of EA treatment for DE and its specific mechanism of action on the Nfr2/HO-1 pathway remain unclear. Male Wistar rats were randomly assigned to four groups: normal, solvent, model, and EA, with 10 rats per group. A DE rat model was induced by intraperitoneal injection of streptozotocin. EA was applied to stimulate the “Zusanli” (ST36) and “Weiwanxiashu” (EXB3) points bilaterally, alternately for 30 min each, once a day for 4 weeks in the EA group. The rats’ fasting blood glucose(FBG) levels were measured with a glucometer. The Morris water maze was used to evaluate their learning and memory abilities. The morphology of neurons in the CA1 area of the hippocampus was observed by Nissl staining. Detection of protein expression of Nrf2 and HO-1 in the CA1 area of the hippocampus was performed by immunohistochemistry and immunoblotting. EA treatment reduced blood glucose levels, improved learning and memory abilities, increased the number of neurons in the hippocampal CA1 area, and upregulated the expression of Nrf2 and HO-1 in rats with DE. EA treatment may inhibit oxidative stress by modulating the Nrf2/HO-1 pathway in the hippocampal CA1 area, exerting a protective effect on neuronal cells in the hippocampal area in DE. EA enhances the learning and memory abilities of rats with DE by regulating the Nrf2/HO-1 pathway in the CA1 area of the hippocampus. This indicates that EA has the potential to protect neurons by reducing oxidative stress.