ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Dapagliflozin mitigates cognitive deficits in a rat model of chronic restrained stress by addressing insulin resistance and mitochondrial dysfunction.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Protective effect of dapagliflozin against phenytoin-induced cerebellar dysfunction and histological alterations in rats: the role of SIRT1/Nrf2/HO-1 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Dapagliflozin ameliorates Alzheimer's disease in rats via stimulating the protective arm of renin angiotensin system and suppressing neuroinflammation.Inflammopharmacology · 2026Article
- Mechanistic Links Between the Gut Microbiome and Longevity Therapeutics.Biomedicines · 2026Review
- The Potential Role of SGLT2 Inhibitors in the Treatment of Depression: Mechanisms and Clinical Prospects.Drug design, development and therapy · 2026Review
- The use of SGLT2 inhibitors in older people: What is important?Aging clinical and experimental research · 2025Review
- TLR-4/Notch1/NF-κB pathway modulation by dapagliflozin: a novel mechanism for neuroprotection in hepatic encephalopathy.Metabolic brain disease · 2025Article
- Dapagliflozin Ameliorates Doxorubicin-Induced Chemobrain and Cognitive Abnormalities in Rats: Modulation of AKT/GSK-3β and Wnt/β-Catenin Pathways.Neurochemical research · 2025Article
- Mechanisms underlying cognitive impairment and management strategies in type 2 diabetes.Frontiers in endocrinology · 2025Review
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7 authors.
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Abstract
Chronic stress is recognized as a risk factor for neurodegeneration. Sodium glucose co-transporter 2 receptors (SGLT2) have been found in various brain regions, suggesting the potential neuroprotective properties of SGLT2 inhibitors as dapagliflozin (DGF). This study aimed to investigate the effect of DGF on behavioral, and neurodegenerative changes in chronic restraint stress (CRS) as an animal model of cognitive impairment. Forty-eight male rats were allocated into four groups: Control; CRS-subjected group, rats were subjected to chronic restraint stress for 6 weeks to induce cognitive impairment; DGF-treated CRS group, dapagliflozin was given daily by oral gavage; and DGF-administered group. Behavioral tests were performed and fasting serum glucose, insulin, and corticosterone levels were measured. Hippocampal oxidative markers, insulin signaling, mitochondrial function, amyloid beta, p-tau, and brain-derived neurotrophic factor (BDNF) gene expression were evaluated. DGF significantly prevented CRS-induced cognitive dysfunction (Y maze and Morris water maze tests). Also, DGF ameliorated hippocampal neurodegenerative changes by decreasing tau and amyloid beta levels, while increasing BDNF gene expression. DGF reduced hippocampal phosphorylated mammalian target of rapamycin (p-mTOR) and protein kinase B (p-Akt) levels. In addition to its antioxidant effects, DGF increased ATP levels and cytochrome C oxidase activity. These findings were confirmed by transmission electron microscopic (TEM) examination. The current study demonstrates a biological link between chronic stress, insulin resistance, and cognitive impairment. Dapagliflozin has therapeutic potential in alleviating cognitive deficits and neurodegeneration primarily due to its insulin-sensitizing and antioxidant properties, along with its capacity to enhance mitochondrial function.
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