ArticleAdvanced pharmaceutical bulletin2025
Investigating the Role of Empagliflozin in the Pathological Progress of Ischemia-Reperfusion Injury in Rat Kidneys: The Involvement of Nitric Oxide.
Article in Advanced pharmaceutical bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency.Journal of cardiovascular translational research · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Renal ischemia-reperfusion (RIR) is a pathological condition that can lead to severe outcomes due to damage to kidney structures. Additionally, oxidative stress is triggered by mitochondrial disruption during reperfusion, potentially resulting in necrosis and, ultimately, cell death through the destruction of cellular membranes. Methods: Thirty rats were included in this study and divided into the following groups: healthy rats, an ischemia-reperfusion (I/R) group, an I/R group treated with empagliflozin, an I/R group treated with empagliflozin plus L-NAME, and an I/R group treated with empagliflozin plus L-arginine. The drugs were administered from three days before I/R induction to one day post-operation. Blood samples were collected 24 hours after I/R induction to evaluate renal function, inflammatory markers, and oxidative stress. Subsequently, the right kidney was harvested for nitric oxide (NO) measurement, while the left kidney was used for histological analysis. Results: Empagliflozin administration significantly reduced creatinine, urea, inflammatory markers, and oxidative stress levels. Moreover, empagliflozin increased the levels of antioxidant enzymes and NO. Histopathological analysis indicated that empagliflozin mitigated ischemia-reperfusion injury in renal tissue. The protective effects were further enhanced with the co-administration of empagliflozin and L-arginine. In contrast, simultaneous treatment with empagliflozin and L-NAME led to pathological changes associated with ischemia-reperfusion and attenuated the beneficial effects of empagliflozin. Conclusion: The findings of this study suggest that empagliflozin exerts protective effects against ischemia-reperfusion injury, likely through the NO pathway.
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