Abstract
Chronic kidney disease (CKD) becomes a global health problem with high morbidity and mortality. Adriamycin- (ADR-) induced rodent chronic nephropathy is a classic experimental model of human minimal lesion nephrotic syndrome. The present study investigated the effect of cobrotoxin (CTX) on ADR-induced nephropathy. Rats were given 6 mg/kg ADR once through the tail vein to replicate ADR nephropathy model. CTX was administered to rats daily by placing a fast dissolving CTX membrane strip under the tongue starting from 5 days prior to ADR administration until the end of experiment. The results showed that CTX ameliorated the symptoms of ADR nephropathy syndrome with reduced body weight loss, proteinuria, hypoalbuminemia, dyslipidemia, serum electrolyte imbalance, oxidative stress, renal function abnormities, and kidney pathological lesions. Anti-inflammatory cytokine IL-10 expression was elevated after CTX administration in ADR nephropathy model. CTX inhibited the phosphorylation of IκB-α and NF-κB p65 nuclear translocation. Meanwhile, CTX upregulated the protein level of podocyte-specific nephrin and downregulated the level of fibrosis-related TGF-β. These findings suggest that CTX may be a potential drug for chronic kidney diseases.
Highlights
Chronic kidney disease (CKD) is recognized as a significant global health problem, owing to its high prevalence and fatality rate [1]
Proteinuria is a clinical indicator of many renal diseases that may be related to podocyte injury
The mean urinary protein excretion was 80.22 ± 32.47 mg/24 h on day 7 after ADR injection in CTX group administrated with 5 μg/kg CTX (P < 0.05, versus model group), and the mean output proteinuria was 245.19 ± 82.42 mg/24 h on day 14 after ADR administration in rats treated with 45 μg/kg CTX (P < 0.05, versus model group)
Summary
Chronic kidney disease (CKD) is recognized as a significant global health problem, owing to its high prevalence and fatality rate [1]. The ADR-induced nephropathy is characterized by massive proteinuria, hypoalbuminemia, dyslipidemia, edema, and abnormal renal functions [5]. ADR-induced chronic nephropathy is the most typical and commonly used experimental model of human minimal lesion nephrotic syndrome [6]. Inflammatory reactions and excessive reactive oxygen species (ROS) production are reported to participate in ADR-induced chronic nephropathy [7, 8]. Proteinuria, which is a biomarker of renal diseases progression, may be associated with the damage of podocyte structure. Podocyte foot processes acted as the main component of glomerular filtration barrier preventing excessive proteins from leaking out [10, 11]. Nephrin protein was identified in SD and participated in maintaining the structure and function of podocytes [13]
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