Puromycin-induced kidney injury and subsequent regeneration in adult zebrafish

Koun, Soonil; Park, Hye-jin; Jung, Su-min; Joo, Jin; Ryong, Dae; Kang, Young Sun

doi:10.1080/19768354.2023.2203211

Cited by 1 publication

(1 citation statement)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Toxic drugs as well as genetic modification in rodents have been extensively used to define mechanisms of disease progression [1]. Toxins such as adriamycin and puromycin induce proteinuric nephropathy such as podocyte injury of nephrotic syndrome [2][3][4][5]. The anthracyclines, including daunorubicin and its 14-hydroxy derivative doxorubicin (adriamycin), are widely used agents in the treatment of cancer, but the cardiotoxicity and nephrotoxicity limit its potential for use.…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Does Not Protect against Adriamycin-Induced Kidney Injury in Mice

Cha,

Park,

Yoo

et al. 2024

Kidney Blood Press Res

View full text Add to dashboard Cite

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. Interstingly, 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.

show abstract