Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi
Protective Effects of Viburnum opulus L. (Gilaburu) on Amiodarone-Induced Hepatorenal Toxicity in Rats
By Dilek Bayram, Nazife Karakeçi and Şükriye Yeşilot.
Abstract
Objective Amiodarone is a widely prescribed antiarrhythmic agent, yet hepatotoxic and nephrotoxic side effects frequently limit its clinical use. Viburnum opulus L. (Gilaburu), a fruit native to the Kayseri region of Türkiye, is notable for its antioxidative, antiproliferative, and anti-inflammatory properties. Its rich composition of organic acids, phenolic compounds, amino acids, and vitamins suggests potential protective effects against drug-induced organ injury. Material and Method This study investigated the structural and biochemical changes induced by amiodarone in rat liver and kidney tissues, as well as the potential protective effects of gilaburu. Thirty-two male Wistar rats (300–350 g) were randomly assigned to four groups: control, amiodarone, amiodarone plus gilaburu, and gilaburu. Amiodarone was administered intraperitoneally at 100 mg/kg/day for 10 days, while gilaburu fruit extract was given orally at 100 mg/kg/day. At the end of treatment, hepatic and renal tissues were analyzed histochemically and immunohistochemically, and serum biochemical parameters were assessed. Results Histological evaluation revealed pronounced hepatic and renal damage in the amiodarone group, which was markedly reduced in the combined treatment group. Immunohistochemical staining for tumor necrosis factor- alpha and inducible nitric oxide synthase showed significantly higher expression in the amiodarone group compared with the combined group (p < 0.05). Biochemical analyses, including total antioxidant status, total oxidant status, and oxidative stress index, supported these findings. Conclusion Gilaburu fruit extract demonstrated significant protective effects against amiodarone-induced hepatic and renal injury. These results highlight its potential as a natural antioxidant agent that may mitigate drug-induced organ toxicity.










