ArticleInternational journal of clinical and experimental pathology2024
Neuroprotective effect of sulforaphane on hyperglycemia-induced cognitive dysfunction through the Nrf2/HO-1 pathway.
Article in International journal of clinical and experimental pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Research Progress on Pathology, Molecular Mechanisms, and Intervention Strategies of Cognitive Dysfunction Associated with Type 2 Diabetes.International journal of general medicine · 2026Review
- Activation of Nrf2 signaling and suppression of oxidative stress-induced neuronal apoptosis: mechanisms for baicalin capsules relieving diabetic encephalopathy.Frontiers in pharmacology · 2026Article
- Characteristics of the Fatty Acid Composition in Elderly Patients with Occupational Pathology from Organophosphate Exposure.Diagnostics (Basel, Switzerland) · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesSulforaphane (SFN), an isothiocyanate in cruciferous plants, has been reported to be effective in treating central nervous system diseases. However, how SFN protects the central nervous system needs further study. The aim of this study was to investigate the neuroprotective effect of SFN and its possible mechanism of action.
methodsSprague-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.
resultsSFN 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.
conclusionsSFN 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.
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