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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 609745, 8 pages
Research Article

Oat Protects against Diabetic Nephropathy in Rats via Attenuating Advanced Glycation End Products and Nuclear Factor Kappa B

Department of Biochemistry, Faculty of Science, King Abdulaziz University, P.O. Box 80203, Jeddah 21589, Saudi Arabia

Received 26 February 2013; Revised 5 September 2013; Accepted 5 September 2013

Academic Editor: Ravirajsinh Jadeja

Copyright © 2013 Abdulrahman L. Al-Malki. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oat, a rich source of soluble fiber, was considered to have a possible preventive effect on the progression of diabetic nephropathy. The present study aimed to assess this preventive activity in a rat model of diabetic nephropathy. Adult Wister rats were injected by streptozotocin (65 mg/kg). Animals were fed with normal diet or with a diet containing 20% oat (W/W) for 21 weeks. At the end of 21 weeks, all the kidney tissues were collected for various examinations. Our results suggested that oat could decrease the Scr and glucose level in blood of diabetic rats significantly ( ), and increase the creatinine clearance ( ). In histopathological examination, oat-fed rats showed a significant decrease in glomerulus segmented sclerosis and incidence of tubule vacuolar degeneration. By ELISA, we reported that oat feeding resulted in decreasing the levels of IL-6 and AGE in serum and kidney homogenate. In addition, the levels of oxidative stress markers were markedly improved as a result of oat feeding. Furthermore, using EMSA, we showed that oat attenuated the activation of NF- B. Using RT-PCR, we found that oat could downregulate the TGF- 1 and RAGE expression at mRNA levels. This study suggests that oat can suppress diabetic nephropathy in rats effectively and may slow down the renal fibrosis by the disruption of the detrimental AGE-RAGE-NF B axis.