In kidney disease, inflammation and lipid dysmetabolism are often associated together, however, the effect and mechanism of inflammatory mediators and lipid dysmetabolism on kidney damage is still unclear. In this study, Wistar rats were randomized into four groups: normal diet + saline (Group N), high-fat diet (HF)+ saline (Group HF), normal diet + adriamycin (Group ADR), HF + adriamycin (Group ADR + HF). After 10 weeks of feeding, rats in each group were randomly sacrificed. We found that the protein content of urine in ADR and ADR + HF groups were significantly higher than that of group N and HF while the serum levels of total protein and albumin in the ADR and ADR + HF groups decreased correspondingly. The serum levels of triglyceride, total cholesterol and low-density lipoprotein in the HF, ADR and ADR + HF groups increased. In the treatment groups, mesangial proliferation, matrix accumulation, tubular vacuolization, inflammatory cell infiltration and fat deposition were detected. These pathological changes were the most serious in the ADR + HF group. The expression of tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) were increased in each treatment group, especially in the ADR + HF group. Our results suggested that the inflammatory factors and abnormal lipid levels can activate the inflammatory response in kidney of the Wistar rats, and lead to a series of pathological changes in renal tissue, and inflammatory factors and lipid dysmetabolism can aggravate damage in the kidney.
Keywords: Adriamycin; lipid; nephrosis; transforming growth factor-β1 (TGF-β1); tumor necrosis factor-α (TNF-α).