Sesame oil prevents acute kidney injury induced by the synergistic action of aminoglycoside and iodinated contrast in rats

Abstract

The aim of the study was to investigate the effect of sesame oil on acute kidney injury induced by the synergistic action of aminoglycoside and iodinated contrast in rats. Acute kidney injury was induced by a 5-day course of daily gentamicin injections (100 mg/kg of body weight, subcutaneously) and then iodinated contrast (4 ml/kg, intravenously) in male specific-pathogen-free Sprague-Dawley rats. Sesame oil (0.5 ml/kg, orally) was given 1 h before iodinated contrast. Renal function and oxidative stress were assessed 6 h after iodinated contrast injection. Renal function was evaluated by measuring serum blood urea nitrogen and creatinine levels. Renal oxidative stress was assessed by determining renal lipid peroxidation, myeloperoxidase, hydroxyl radical, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase levels. Sesame oil significantly prevented the rise of serum blood urea nitrogen and creatinine levels. Furthermore, there was a parallel inhibition of the rise in levels of expression of renal lipid peroxidation, myeloperoxidase, hydroxyl radicals, superoxide anion, nitrite/nitrate, and inducible nitric oxide synthase in rats with gentamicin-plus-iodinated contrast-induced acute kidney injury. We conclude that sesame oil may attenuate aminoglycoside-plus-iodinated contrast-induced acute kidney injury by inhibiting renal oxidative stress in rats.

Fig. 1.

Effects of sesame oil on gentamicin-plus-iodinated contrast-induced acute kidney injury in rats. Rats were divided into five groups, and BUN (A) and creatinine (B) levels were determined 6 h after contrast injection. Data are expressed as means ± SDs (n = 6). Significant differences of measurement traits were analyzed using one-way ANOVA, followed by Tukey HSD post hoc analysis. *, P < 0.05 compared with G group; †, P < 0.05 compared with CG group.

Fig. 2.

Effect of sesame oil on histological changes in gentamicin-plus-iodinated contrast-induced acute kidney injury. Rats were divided into five groups, and histological changes were examined 6 h after contrast injection. The arrows indicate hyaline deposits with renal tubular cell necrosis. Hematoxylin and eosin stain. Magnification = ×100. For histopathological score, data are expressed as means ± SDs (n = 6). Significant differences of measurement traits were analyzed using one-way ANOVA, followed by Tukey HSD post hoc analysis. *, P < 0.05 compared with G group; ††, P < 0.01 compared with CG group.

Fig. 3.

Effect of sesame oil on oxidative stress in gentamicin-plus-iodinated contrast-induced acute kidney injury. Rats were divided into five groups, and lipid peroxidation (A) and myeloperoxidase (MPO) (B) levels were determined 6 h after contrast injection. Data are expressed as means ± SDs (n = 6). Significant differences of measurement traits were analyzed using one-way ANOVA, followed by Tukey HSD post hoc analysis. MDA, malondialdehyde; *, P < 0.05 compared with G group; †, P < 0.05 compared with CG group; ††, P < 0.01 compared with CG group.

Fig. 4.

Effect of sesame oil on oxygen free radical generation in gentamicin-plus-iodinated contrast-induced acute kidney injury. Rats were divided into five groups, and renal hydroxyl radical (A) and superoxide (B) levels were determined 6 h after contrast injection. Data are expressed as means ± SDs (n = 6). Significant differences of measurement traits were analyzed using one-way ANOVA, followed by Tukey HSD post hoc analysis. *, P < 0.05 compared with G group; †, P < 0.05 compared with CG group; ††, P < 0.01 compared with CG group.

Fig. 5.

Effect of sesame oil on nitric oxide and iNOS expression in gentamicin-plus-iodinated contrast-induced acute kidney injury. Rats were divided into five groups, and the renal nitrite/nitrate level (A) and iNOS expression (B) were determined 6 h after contrast injection. Data are expressed as means ± SDs (n = 6). Significant differences of measurement traits were analyzed using one-way ANOVA, followed by Tukey HSD post hoc analysis. *, P < 0.05 compared with G group; †, P < 0.05 compared with CG group; ††, P < 0.01 compared with CG group.