ArticleNaunyn-Schmiedeberg's archives of pharmacology2019
Effect of canagliflozin, a sodium glucose co-transporter 2 inhibitor, on cisplatin-induced nephrotoxicity in mice.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- From molecules to the clinic-pathophysiology of sodium-glucose cotransporter 2 inhibitors and their emerging role in urology: A comprehensive review from the European Association of Urology Section of Endourology.Asian journal of urology · 2026Review
- Beneficial Effects of Sodium-Glucose Cotransporter 2 Inhibitors in Cisplatin Nephrotoxicity: A Mechanistic Review.Kidney360 · 2026Review
- Dapagliflozin treatment ameliorates oxidative stress, apoptosis and inflammation in tenofovir-induced nephrotoxicity in rats.Scientific reports · 2025Article
- Canagliflozin potentially promotes renal protection against glycerol-induced acute kidney injury by activating the AMPK/SIRT1/FOXO-3a/PGC-1α and Nrf2/HO-1 pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Sodium-Glucose Cotransporter 2 Inhibitors: Guarding Against Cisplatin-Associated Magnesium Wasting and Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- The Effect of Dapagliflozin, a Sodium-Glucose Co-Transporter 2 Inhibitor, on Vancomycin-Induced Nephrotoxicity in Rats.Biomedicines · 2025Article
- Acute Cisplatin Nephrotoxicity, Sodium-Glucose Cotransporter 2 Inhibitors, and Benefits Beyond Magnesium.Journal of the American Society of Nephrology : JASN · 2025Article
- Canagliflozin alleviates acetaminophen-induced renal and hepatic injury in mice by modulating the p-GSK3β/Fyn-kinase/Nrf-2 and p-AMPK-α/STAT-3/SOCS-3 pathways.Scientific reports · 2025Article
- Advances in sodium-glucose transporter protein 2 inhibitors and tumors.Frontiers in oncology · 2025Review
- Palliative effects of carnosol on lung-deposited pollutant particles-induced thrombogenicity and vascular injury in mice.Pharmacology research & perspectives · 2024Article
- Sodium Glucose Cotransporter-2 Inhibitors in Non-Diabetic Kidney Disease: Evidence in Experimental Models.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Sodium-Glucose Co-Transporter 2 Inhibitors: Mechanism of Action and Efficacy in Non-Diabetic Kidney Disease from Bench to Bed-Side.Journal of clinical medicine · 2024Review
- SGLT2 inhibitor dapagliflozin protects the kidney in a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2024Article
- Canagliflozin ameliorates high glucose-induced apoptosis in NRK-52E cells via inhibiting oxidative stress and activating AMPK/mTOR-mediated autophagy.Molecular biology reports · 2023Article
- Canagliflozin retards age-related lesions in heart, kidney, liver, and adrenal gland in genetically heterogenous male mice.GeroScience · 2023Article
- Canagliflozin alleviates valproic acid-induced autism in rat pups: Role of PTEN/PDK/PPAR-γ signaling pathways.Frontiers in pharmacology · 2023Article
- The Nephroprotective Effects of α-Bisabolol in Cisplatin-Induced Acute Kidney Injury in Mice.Biomedicines · 2022Article
- Renal outcomes with sodium-glucose cotransporters 2 inhibitors.Frontiers in endocrinology · 2022Review
- Effects of repeated increasing doses of cisplatin as models of acute kidney injury and chronic kidney disease in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Canagliflozin is a sodium glucose co-transporter 2 (SGLT2) inhibitor that is currently available for the management of type 2 diabetes mellitus. The present study investigated the effect of canagliflozin on cisplatin (CP)-induced nephrotoxicity in mice. The animals were divided into four groups (n = 6). The first and second groups received normal saline (control) and intraperitoneal (i.p.) cisplatin (20 mg/kg) on day 7, respectively. The third and fourth groups were given a single intraperitoneal (i.p.) injection of CP (20 mg/kg) on day 7 and canagliflozin (10 mg/kg/day) and (30 mg/kg/day), for 10 days, respectively. At day 11, animals were anesthetized and blood collected and kidneys were removed. CP significantly increased the plasma urea, creatinine, cystatin C, and clusterin concentrations and neutrophil gelatinase-associated lipocalin (NGAL) activity. In addition, CP increased urinary albumin/creatinine ratio, N-acetyl-β-D-glucosaminidase (NAG) activity, and liver-type fatty acid-binding protein (L-FABP) concentrations and reduced creatinine clearance. CP also significantly increased the plasma concentration of inflammatory cytokines [plasma tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1beta (IL-1β)] and significantly reduced antioxidant indices [catalase, glutathione reductase (GR), and superoxide dismutase (SOD)]. Histopathologically, CP caused a remarkable renal damage compared with control. Canagliflozin significantly ameliorated CP-induced biochemical and histopathological changes. The protective effect of canagliflozin is most likely due to anti-inflammatory and antioxidant effects. Our results show that administration of canagliflozin reversed the biochemical and histopathological indices of CP-induced nephrotoxicity in mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.