Abstract: SA-PO0248
Protective Effects of Sodium Pentaborate Against Cyclosporine A-Induced Nephrotoxicity
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Ozkan, Gulsum, Tekirdag Namik Kemal Universitesi, Tekirdag, Istanbul, Turkey
- Ulusoy, Sukru, Karadeniz Teknik Universitesi, Trabzon, Turkey
- Kara, Sonat Pinar, Tekirdag Namik Kemal Universitesi, Tekirdag, Istanbul, Turkey
- Karabag, Sevil, Tekirdag Namik Kemal Universitesi, Tekirdag, Istanbul, Turkey
- Celikkol, Aliye, Tekirdag Namik Kemal Universitesi, Tekirdag, Istanbul, Turkey
Background
Cyclosporine A (CsA), a calcineurin inhibitor widely used in transplantation and glomerular diseases, is limited by nephrotoxicity largely driven by oxidative stress. Sodium pentaborate (NaPB), a bioavailable boron compound, has shown antioxidant and cytoprotective effects. This study evaluated the protective role of NaPB against CsA-induced nephrotoxicity.
Methods
Twenty-eight female Sprague–Dawley rats were randomized into four groups (n=7): Control, NaPB (100 mg/kg/day), CsA (25 mg/kg/day), and CsA+NaPB. Treatments were given by oral gavage for 21 days. Renal function was assessed by serum blood urea nitrogen (BUN) and creatinine. Oxidative stress was evaluated using total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and malondialdehyde (MDA). Histopathological analysis was also performed.
Results
CsA significantly increased creatinine and BUN compared to controls (p=0.009 and p=0.017). TOS, OSI, and MDA levels were elevated, while TAS decreased in the CsA group (p<0.05). Co-treatment with NaPB significantly reduced creatinine and MDA (p=0.009 and p=0.002) and markedly improved histopathological damage (p=0.001), restoring values close to control levels. Although TOS and OSI decreased with NaPB, these changes were not statistically significant.
Conclusion
NaPB attenuates CsA-induced renal dysfunction, oxidative stress, and tissue injury, suggesting oxidative stress modulation as a therapeutic target and NaPB as a promising renoprotective adjunct.