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The Effect of Dapagliflozin, a Sodium-Glucose Co-Transporter 2 Inhibitor, on Vancomycin-Induced Nephrotoxicity in
Seyhmus Tan1, Bulent Kaya2, Ercan Akburak1
1Department of Internal Medicine, Faculty of Medicine, Çukurova University, 01330 Adana, Sarıçam, Turkey.
Abstract:
Background/Objectives: Vancomycin-induced nephrotoxicity (VIN) remains a significant clinical challenge, with no effective nephroprotective agent currently established. This study aimed to evaluate the protective effects of the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (DAPA) against VIN in a Wistar albino rat model. Methods: Rats were randomly assigned to four groups: control, VA (vancomycin), DAPA (dapagliflozin), and VA+DAPA. Renal function was assessed by measuring serum urea and creatinine. Oxidative stress markers [malondialdehyde (MDA), total oxidant status (TOS), and myeloperoxidase (MPO)], antioxidant enzyme activities [total antioxidant status (TAS), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD)], apoptotic mediators (Bax, Bcl-2, and caspase-3), and pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6)] were evaluated. Histopathological and immunohistochemical analyses of kidney tissues were also performed. Results: Administration of VA led to significant renal dysfunction, increased oxidative stress, heightened apoptotic activity, and notable histopathological damage. Co-administration of DAPA with VA significantly reduced serum urea and creatinine levels and decreased caspase-3 activity and was associated with a trend toward reduction in both MDA levels and TNF-α expression, as well as the amelioration of histopathological renal injury. However, reductions in IL-1β and IL-6 levels were not statistically significant. Overall, these findings indicate that DAPA exerts nephroprotective effects against VIN by modulating oxidative stress, inflammation, and apoptotic pathways. Conclusions: Dapagliflozin may serve as a potential protective agent against vancomycin-induced nephrotoxicity. Further long-term and large-scale clinical studies are warranted to validate these preclinical findings and explore their therapeutic implications.
Insights
Dapagliflozin shows promise in protecting against vancomycin-induced nephrotoxicity by reducing kidney damage markers and oxidative stress. Further clinical studies are needed to confirm its protective role in patients.
Area of Science:
- Nephrology
- Pharmacology
- Toxicology
Background:
- Vancomycin-induced nephrotoxicity (VIN) is a significant clinical problem with no established nephroprotective agents.
- Sodium-glucose cotransporter 2 (SGLT2) inhibitors, like dapagliflozin, are being investigated for potential renal protective effects.
Purpose of the Study:
- To evaluate the nephroprotective effects of dapagliflozin (DAPA) against vancomycin-induced nephrotoxicity (VIN) in a Wistar albino rat model.
- To assess the impact of DAPA on renal function, oxidative stress, apoptosis, and inflammation markers in VIN.
Main Methods:
- Wistar albino rats were divided into control, vancomycin (VA), dapagliflozin (DAPA), and VA+DAPA groups.
- Renal function (serum urea, creatinine), oxidative stress, antioxidant enzymes, apoptotic mediators, and pro-inflammatory cytokines were measured.
- Histopathological and immunohistochemical analyses of kidney tissues were conducted.
Main Results:
- Vancomycin administration induced significant renal dysfunction, oxidative stress, apoptosis, and kidney damage.
- Co-administration of dapagliflozin with vancomycin significantly reduced serum urea and creatinine, decreased caspase-3 activity, and showed trends toward reduced MDA and TNF-α.
- Dapagliflozin improved histopathological renal injury, although IL-1β and IL-6 reductions were not significant.
Conclusions:
- Dapagliflozin demonstrates nephroprotective effects against vancomycin-induced nephrotoxicity in rats.
- These effects are mediated by the modulation of oxidative stress, inflammation, and apoptotic pathways.
- Further clinical research is warranted to validate dapagliflozin's potential as a nephroprotective agent against VIN.
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