Soy protein prevents renal damage in a fructose-induced model of metabolic syndrome via inhibition of NF-kB in male rats.

The study determines the effect of soy protein on inflammatory status and expression of nuclear factor-kappa B (NF-κB P(65)) and receptor for advanced glycation end products (RAGE) in a metabolic syndrome (MS) model. MS was induced in adult male rats by feeding them a high fructose diet (60 g/100 g diet). The rats were randomised into six groups by feeding one of the following semi-synthetic diets for 60 days: corn starch (60%) and casein (20%; CCD), fructose (60%) and casein (20%; FCD), fructose (60%) and soy protein (20%; FSD) or corn starch (60%) and soy protein (20%; CSD). The expression of NF-κB P(65), transforming growth factor-β1 (TGF-β1) and RAGE, histochemical localization of α-smooth muscle actin (α-SMA), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) assays, collagen deposition and ultrastructural analysis were performed. FCD rats displayed inflammatory changes and increased expression of growth factors and nuclear factors. FSD rats showed reduction in inflammation, fibrogenesis, collagen deposition, NF-κB activation and mitigated the ultrastructural changes. Soy protein prevents inflammation and early nephropathic changes in the MS model secondary to the attenuation of NF-κB activation.