RETRACTED ARTICLE: Soy protein prevents renal damage in a fructose-induced model of metabolic syndrome via inhibition of NF-kB in male rats
Authors: Carani Venkataraman Anuradha
Nallasamy Palanisamy
Journal: Pediatric Nephrology (2011)
Discipline: CLINICAL MEDICINE
Keywords: soy protein; inflammatory status; nuclear factor-kappa B; NF-Œ∫B P(65); receptor for advanced glycation end products
Affiliations: Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar, 608 002 Tamil Nadu, India. 

Abstract:  The study determines the effect of soy protein on inflammatory status and expression of nuclear factor-kappa B (NF-Œ∫B 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-Œ∫B P(65), transforming growth factor-Œ≤1 (TGF-Œ≤1) and RAGE, histochemical localization of Œ±-smooth muscle actin (Œ±-SMA), tumour necrosis factor-Œ± (TNF-Œ±) 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-Œ∫B activation and mitigated the ultrastructural changes. Soy protein prevents inflammation and early nephropathic changes in the MS model secondary to the attenuation of NF-Œ∫B activation. 

Retracted: No

PubPeer comments:
 Erratum retraction published [January 19 2013] :  **Erratum to: Pediatr Nephrol**  DOI 10.1007 s00467-011-1882-1  The core data and conclusions were published before in another journal: Eur J Pharmacol (2011 Sep 30; 667:355u201364). There is considerable overlap in the main sections. The previous paper containing the core data and conclusions was  **Genistein** modulates NF-u03baB-associated renal inflammation, fibrosis and podocyte abnormalities in fructose-fed rats [(Palanisamy et al (2011)] . That is, the data and core conclusions were not only recycled, but re-purposed to describe soy protein rather than genistein. Fig 7 of the present paper suggests that its problems go further than repurposing: Areas of copy-pasted tissue in the FSD and CSD rows are marked.   Analysis of NF-u03baB P65 expression in the kidney of experimental rats by confocal imaging. Tissue sections were immunostained with the anti-NF-u03baB P65 antibody and an FITC-conjugated secondary antibody (green). Counterstaining was performed using propidium iodide (PI; red). Images were visualised using a confocal microscope at magnification u00d740. Renal cells from the CCD group remained negative for both NF-u03ba B-FITC and PI staining. Renal cells from FCD group stained positive from NF-u03ba B-FITC and PI staining and renal cells from the FSD group expression was significantly lowered. , 
 [Below] Fig 1(a):  Representative immunoblots showing the expression of NF-u03ba B P65 in kidney cytosol (a) , for various combinations of high-fructose diet and **soy protein**. [Above] Fig. 2 from [Nallasamy Palanisamy Anuradha C. Venkataraman (2013)] .  Representative immunoblot of protein kinase C-bII (PKC-bII) isoenzyme in kidney (a) cytosol and (b) membrane for various combinations of high-fructose diet and **genistein**.  The loading controls appear to be the same despite differences in conditions. ,