Nephrotoxicity, characterized by adverse effects on renal function and structural damage, is a common consequence of exposure to various drugs and toxins, including chemotherapeutic agents such as Cisplatin. Mechanisms explored include drug accumulation in renal cells via transporters like Ctr1 and OCT2, oxidative stress driven by reactive oxygen species (ROS), inflammation mediated by NF-κB, lipid peroxidation and activation of apoptotic pathways involving Bcl-2, Bax and caspases. To counter cisplatin nephrotoxicity, oral hypoglycemic agents exhibit nephroprotective potential. Sulfonylureas (glibenclamide, gliclazide, glimepiride) modulate oxidative enzymes and inflammatory pathways. Metformin, a biguanide, exerts pleiotropic effects, including anti-inflammatory and antioxidant actions. Thiazolidinediones (rosiglitazone, pioglitazone) demonstrate anti-inflammatory properties, safeguarding against cisplatin-induced renal injury. Sodium-glucose cotransporter-2 (SGLT2) inhibitors (canagliflozin, empagliflozin) offer mitochondrial protection and apoptosis suppression. Dipeptidyl-peptidase IV (DPP-4) inhibitors (sitagliptin, saxagliptin, linagliptin) showcase antioxidant and anti-inflammatory effects, attenuating cisplatin-induced renal damage. This comprehensive understanding provides insights for potential strategies to mitigate cisplatin nephrotoxicity and enhance the safety of cancer treatments.
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