ArticleMetabolic brain disease2025
Neuroprotective effects of Saxagliptin in traumatic brain injury: ameliorating oxidative stress, neuroinflammation, and apoptosis.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Apigenin Mitigates PFOA-Induced Activation of the NLRP3-Pyroptosis Axis and Associated Neurological Damage.Environment & health (Washington, D.C.) · 2026Article
- From glycemic control to neuroprotection: alogliptin as a repurposed candidate for Huntington's disease.Metabolic brain disease · 2026Review
- Neuronal Injury and Regeneration-Linked Gene Expression Dynamics in the Hypothalamic-Pituitary-Adrenal Axis Following Experimental Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Traumatic brain injury induces DNA damage in Drosophila.microPublication biology · 2025Article
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4 authors.
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Abstract
Traumatic Brain Injury (TBI) is a significant global health issue characterized by disruptions in normal brain function due to external mechanical forces. Saxagliptin, a Dipeptidyl Peptidase-4 (DPP-4) inhibitor primarily used for diabetes management, has demonstrated potential anti-inflammatory effects that may offer therapeutic benefits for Central Nervous System (CNS) disorders. Using a network pharmacology approach, we identified Saxagliptin's molecular targets relevant to TBI pathology. Male Sprague Dawley rats were subjected to TBI via a weight-drop method and were randomly assigned to one of four groups (n = 10 per group): sham, TBI + vehicle, TBI + Saxagliptin (1 mg/kg/day), and TBI + Saxagliptin (3 mg/kg/day). Neuroprotective effects were assessed through neurobehavioral tests, brain water content measurement, biochemical assays for oxidative stress and inflammatory markers, and histopathological analysis of brain tissue. Network pharmacology identified 49 intersecting targets between Saxagliptin and TBI, with key roles in apoptosis and neuroinflammation pathways. In vivo results revealed that saxagliptin treatment markedly improved neurobehavioral outcomes. Histological analysis showed a decrease in neuronal cell death following Saxagliptin treatment. Biochemical assessments revealed that Saxagliptin mitigated TBI-induced oxidative stress markers, including oxidative DNA damage. Furthermore, Saxagliptin attenuated neuroinflammation, as shown by reduced levels of iNOS, COX-2, IL-6, and TNF-α, and ameliorated blood-brain barrier (BBB) damage. Additionally, Saxagliptin reduced apoptosis by lowering Bax, Caspase 3 levels and increasing Bcl-2 levels. Saxagliptin exhibits notable neuroprotective effects in TBI by mitigating oxidative stress, reducing neuroinflammation, and preventing neuronal apoptosis. These findings suggest that Saxagliptin could be a viable therapeutic agent for improving outcomes in TBI management.
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