Conclusions
SFN ameliorated diabetes-induced cognitive dysfunction by activating the Nrf2/HO-1 pathway, providing a new perspective for SFN therapy to delay cognitive impairment in diabetes patients.
Methods
Sprague-Dawley rats were used to develop a cognitive impairment model. The Morris water maze (MWM) was used to evaluate the effect of SFN on learning and memory, and haematoxylin-eosin (H&E) staining and terminal transferase deoxyuridine nick-end labelling (TUNEL) were used to observe morphologic changes in neurons and neuronal apoptosis in the hippocampus and cortex. An oxidative stress marker kit was used to detect the content and activity of SFN, and the expressions of nuclear factor drythroid-2 related Factor 2 (Nrf2), heme oxygenase 1 (HO-1), and NAD(P)H quinone oxidoreductase 1 (NQO-1) were measured by RT-PCR.
Results
SFN treatment significantly improved cognition, increased the number of neurons, and suppressed neuronal apoptosis. In addition, SFN significantly decreased the content of malondialdehyde (MDA) and enhanced the antioxidant activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the hippocampus and cortex. Furthermore, SFN elevated the expression of Nrf-2, HO-1, and NQO-1. Conclusions: SFN ameliorated diabetes-induced cognitive dysfunction by activating the Nrf2/HO-1 pathway, providing a new perspective for SFN therapy to delay cognitive impairment in diabetes patients.