Protective effect of sulforaphane on kidney injury in rats with nephrotic syndrome

Abstract

Objective To study the effects of sulforaphane on kidney injury and the expression levels of nitric oxide synthase in rats with nephrotic syndrome. Methods Five mg/kg of doxorubicin was used to construct the nephrotic syndrome model in rats. Rats were divided into control group, model group, sulforaphane treatment group and benazepril (positive drug) treatment group. After treatment with 30 mg/kg of sulforaphane and 6 mg/kg of benazepril for 6 weeks, HE staining was used to analyze pathological changes in kidney tissue in rats with nephrotic syndrome. Proteinuria level in 24 hours was measured by BCA assay. ELISA assay was used to detect the level of plasma albumin. NO content was detected by spectrophotometer. Western blot was used to determine the expression levels of endothelial NOS (eNOS), inducible NOS (iNOS) and neural NOS (nNOS). Results Compared with control group, the 24 hours proteinuria level was significantly increased in model group (P<0.05), and the pathological changes of the kidney were serious. The urine NO content of the model group was greatly decreased (P<0.05), the level of plasma albumin was greatly decreased (P<0.05), and the expression levels of eNOS, iNOS and nNOS were also significantly decreased (P<0.05). Compared with model group, the 24 hours proteinuria level was significantly increased in sulforaphane treatment group and benazepril treatment group group (P<0.05), the level of plasma albumin was greatly increased (P<0.05), and the pathological changes of the kidney were significantly improved. The urine NO content of the treatment groups was greatly increased (P<0.05), and the expression levels of eNOS, iNOS and nNOS were also significantly increased (P<0.05). Conclusions Sulforaphane can improve the expressions of eNOS, iNOS and nNOS in nephrotic syndrome rats, increase the content of NO in rats, reduce the content of urinary protein, and improve the pathological process of nephrotic syndrome. Key words: Models, Animal; Rats; Nephrosis, Lipoid; Sulforaphane