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Dapagliflozin Does Not Protect against Adriamycin-Induced Kidney Injury in Mice
Jin Joo Cha1, Hye-Jin Park1, Ji Ae Yoo1
1Department of Nephrology, Korea University Ansan Hospital, Ansan-si, Republic of Korea.
Introduction:
Sodium-glucose cotransporter 2 (SGLT2) inhibitors target SGLT2 in renal proximal tubules and promote glycosuria in type 2 diabetes mellitus in humans and animal models, resulting in reduced blood glucose levels. Although clinical trials have shown that SGLT2 inhibitors attenuate the progression of chronic kidney disease, there have been concerns regarding SGLT2-induced acute kidney injury. In this study, we investigated the effect of SGLT2 inhibitors on adriamycin-induced kidney injury in mice.
Methods:
Seven-week-old balb/c mice were injected with adriamycin 11.5 mg/kg via the tail vein. Additionally, dapagliflozin was administered via gavage for 2 weeks. The mice were divided into five groups: vehicle, dapagliflozin 3 mg/kg, adriamycin, adriamycin plus dapagliflozin 1 mg/kg, and adriamycin plus dapagliflozin 3 mg/kg.
Results:
Adriamycin injection reduced the body weight and food and water intakes. Dapagliflozin also decreased the body weight and food and water intakes. Fasting blood glucose and urine volume were not altered by either adriamycin or dapagliflozin. Once adriamycin-induced kidney injury had developed, there were no differences in systolic blood pressure among the groups. Dapagliflozin did not alleviate proteinuria in adriamycin-induced kidney injury. Adriamycin induced significant glomerular and interstitial injury, but dapagliflozin did not attenuate these changes in renal injury. Interestingly, SGLT2 expressions were different between the cortex and medulla of kidneys by dapagliflozin treatment. Dapagliflozin increased SGLT2 expression in medulla, not in cortex.
Conclusion:
Dapagliflozin had no effect on proteinuria or inflammatory changes such as glomerular and tubular damages in adriamycin-induced kidney injury. Our study suggests that dapagliflozin does not protect against adriamycin-induced kidney injury. More experimental studies regarding the effects of SGLT2 inhibitors on various kidney diseases are needed to clarify the underlying mechanisms.
Insights
Sodium-glucose cotransporter 2 (SGLT2) inhibitors like dapagliflozin did not protect against adriamycin-induced kidney injury in mice. The study found no improvement in proteinuria or renal damage, suggesting further research is needed.
Area of Science:
- Nephrology
- Pharmacology
- Toxicology
Background:
- Sodium-glucose cotransporter 2 (SGLT2) inhibitors are used to manage type 2 diabetes by promoting glycosuria and lowering blood glucose.
- While beneficial for chronic kidney disease progression, concerns exist about SGLT2 inhibitors potentially causing acute kidney injury.
Purpose of the Study:
- To investigate the protective effects of SGLT2 inhibitors against adriamycin-induced kidney injury in a mouse model.
- To evaluate the impact of dapagliflozin on renal function and histological damage in the context of adriamycin nephrotoxicity.
Main Methods:
- Balb/c mice were administered adriamycin to induce kidney injury.
- Dapagliflozin was administered orally for two weeks at different dosages.
- Mice were divided into vehicle, dapagliflozin, adriamycin, and adriamycin plus dapagliflozin groups for comparison.
Main Results:
- Adriamycin and dapagliflozin reduced body weight and intake of food and water.
- Neither adriamycin nor dapagliflozin affected fasting blood glucose or urine volume.
- Dapagliflozin did not alleviate proteinuria or attenuate glomerular and interstitial injury in adriamycin-induced kidney injury.
- Dapagliflozin increased SGLT2 expression in the kidney medulla but not the cortex.
Conclusions:
- Dapagliflozin demonstrated no protective effect against adriamycin-induced kidney injury, proteinuria, or inflammatory changes.
- The findings suggest that dapagliflozin does not mitigate adriamycin nephrotoxicity in this experimental model.
- Further research is warranted to elucidate the mechanisms of SGLT2 inhibitors in various kidney diseases.
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