Oxidative stress induced generation of reactive oxygen species and other free radicals have been implicated in MetS, pathogenesis of kidney diseases and also in MetSinduced tubulointerstitial injury. Superoxide anions have been shown to cause increased smooth muscle cell contraction by regulating cytosolic calcium concentrations. Our EPR data show that the generation of ROS, superoxide and peroxynitrite were increased in the medulla and cortical tissue of the kidneys of MetS animals. This increase in the mediators of oxidative stress in the kidney tissue can induce vasoconstriction of the arterioles, thus contributing to the decreased RBF and elevated RVR in the MetS animals. Further, the antioxidant defense mechanism in these OZRCC animals were weak compared to the LZRCC and LZRBB rats, as indicated by the SOD and catalase enzyme activity. The BB-enriched diet, however, was able to restore the redox balance in the MetS animals. Obesity and hypertension are hallmarks of MetS that have been implicated in kidney diseases. In addition to the injury to the kidney tissue, proteinuria and microalbuminuria have been linked to MetS-associated CKD. Studies have also shown that glomerulopathy and VE-821 1232410-49-9 injury-induced reduction in the absorption by the tubules result in proteinuria. Our histopathological data clearly indicates a marked disruption of the renal structure in the OZRCC animals compared to the LZR rats. This structural damage in OZRCC animals included glomerular sclerosis, interstitial nephritis, fibrosis and proteinuria. We also examined the gene expression of TGF-b, which is an important profibrotic marker. The OZRCC animals had an elevated expression of TGF-b which was significantly reduced in OZRBB group. Interestingly, previous studies have correlated renal TLR4 expression with the inflammatory marker TGF-b in CKD. An increase in TGF-b mRNA levels has been implicated in the glomeruli of diabetic rats. Further, we also measured the albuminuria levels in these animals and our results were consistent with the histopathological findings. BB was able to exert a reno-protective effect by attenuating nephropathy and albuminuria in OZRBB rats. Inflammation is one of the major contributors to the progression of MetS-induced kidney disorders. TLR4 signaling pathways and their expression have been studied in relation to inflammation in kidney injury. We examined the gene and protein expression of TLR4 in the kidney cortical tissues of animals from all experimental groups. Interestingly, the gene and protein expression of TLR4 was significantly increased in the OZRCC rats compared to the LZRCC and LZRBB groups. The TLR4 signaling-driven inflammation is, at least in part, a possible cause for the progression of glomerular and tubular injury in the MetS animals, thereby contributing to renal dysfunction. The MetS animals that were fed on a BB-diet had a reduced gene and protein expression of TLR4 in the kidney cortex.