L-carnitine mitigates urographin-induced nephrotoxicity via modulation of inflammatory, oxidative, and apoptotic pathways in rat kidney.

Contrast-induced nephropathy (CIN) remains a significant clinical challenge, particularly following the administration of iodinated agents such as urographin. L-carnitine (LC) is a substance known for its anti-inflammatory and antiapoptotic effects. This study investigates the nephroprotective potential of LC through its regulatory effects on inflammation, oxidative stress, and apoptosis in a rat model of CIN. Thirty-two Wistar albino rats were assigned to four groups: Control, urographin (URO, 10 mL/kg i.p.), URO-LC (200 mg/kg L-carnitine i.p. for 10 days), and LC alone. Renal function markers (urea, creatinine), oxidative stress indicators as total oxidans status (TOS), total antioxidant status (TAS), oxidative stress (OSI), and histopathological features were evaluated. The immunohistochemical expression of tumor necrosis factor alpha (TNF-α) and Caspase-3 (Cas-3), along with the mRNA expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and Caspase-9 (Cas-9), were assessed. URO significantly increased serum urea and creatinine levels, TOS and OSI values. TNF-α and Cas-3 immunoreactivity, along with Bax and Cas-9 gene expression, were markedly elevated in the URO group, while anti-apoptotic Bcl-2 expression was suppressed. URO also induced severe histological damage. LC treatment reversed these effects, preserving tissue integrity and restoring molecular markers toward baseline levels. LC exerts potent nephroprotective effects against URO-induced renal injury by attenuating oxidative stress, suppressing pro-inflammatory and apoptotic signaling, and promoting anti-apoptotic gene expression. These findings support its potential clinical use in the prevention of contrast-induced renal damage.