Advancing nephroprotective strategies: the role of naringenin in preventing gentamicin-induced nephrotoxicity

Abstract

Gentamicin-induced nephrotoxicity (GIN) remains a significant clinical challenge due to its association with oxidative stress, inflammation, and mitochondrial dysfunction. Despite its effectiveness as an aminoglycoside antibiotic for treating Gram-negative bacterial infections, gentamicin’s nephrotoxic potential limits its clinical use, affecting 10–20% of patients. In response to these challenges, naringenin, a flavonoid with potent antioxidant and anti-inflammatory properties, has emerged as a promising therapeutic agent for mitigating renal damage. This narrative review explores the multifaceted mechanisms underlying naringenin’s nephroprotective effects, including its ability to neutralize reactive oxygen species (ROS), modulate inflammatory pathways, and enhance cellular repair mechanisms through pathways such as PI3K/Akt and MAPK. Both in vitro and in vivo studies support the capability of naringenin to counteract gentamicin-induced nephrotoxicity by preserving renal function, reducing oxidative stress, and reducing inflammation. While preclinical evidence is robust, further clinical research is essential to establish its efficacy, safety, and optimal dosing in nephrotoxic contexts. This review synthesizes existing data and highlights the need for continued investigation into naringenin as a potential adjunctive therapy in the management of nephrotoxicity.