Vinpocetine Improves Oxidative Stress and Pro‑Inflammatory Mediators in Acute Kidney Injury

Gentamicin‑induced‑acute kidney injury (AKI) is a multifaceted phenomenon which previously linked to the oxidative stress only. Vinpocetine prevents reactive free radical generation which contributed in reduction of damage. Therefore, objective of the present study was to investigate the renoprotective effect of vinpocetine on gentamicin‑induced‑AKI in rats.

 Thirty Sprague Dawley Male rat were divided into three groups. Control group (n </em>= 10): Rats treated with distilled water + intra‑peritoneal injection of normal saline 2 ml/kg/day. Gentamicin group (n </em>= 10): Rats treated with distilled water + intra‑peritoneal injection of gentamicin 100 mg/kg/day. Vinpocetine group (n </em>= 10): Rats treated with vinpocetine + intra‑peritoneal injection of  gentamicin 100 mg/kg/day. Blood urea and serum creatinine were estimated by auto‑analyzer. Serum malondialdehyde (MDA), superoxide dismutase (SOD), Neutrophil Gelatinase Associated Lipocalin (NGAL), kidney injury molecules (KIM‑1), and Cystatin‑c were measured by ELISA kit methods.

Vinpocetine led to significant renoprotective effect on gentamicin induced‑AKI through amelioration of blood urea and serum creatinine compared with gentamicin group P </em>< 0.01. Vinpocetine improved oxidative stress through reduction of MDA serum level and elevation of SOD significantly compared with gentamicin group P </em>= 0.001 and P </em>= 0.03, respectively. Indeed, vinpocetine reduced glomerular and renal tubular injury via reduction of inflammatory biomarkers including KIM‑1, NGALand Cystatin‑c sera levels significantly P </em>< 0.01 compared to gentamicin group.

Vinpocetine leads to significant attenuation of gentamicin‑induced‑AKI through modulation of oxidative stress and pro‑inflammatory pathway.