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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 409047, 10 pages
Research Article

Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT1 Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats

Department of Biological Sciences, Faculty of Science, Kuwait University, P.O. Box 5969, Safat 13060, Kuwait

Received 13 August 2012; Accepted 13 October 2012

Academic Editor: Khalid Rahman

Copyright © 2012 Martha Thomson et al. 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.


This study investigates the potential of green tea to modulate oxidative stress and angiotensin II AT1 receptor expression in renal and hepatic tissues of diabetic rats. Three groups of rats were studied after 8 weeks following diabetes induction: normal, streptozotocin-induced diabetic (diabetic control), and green-tea-treated diabetic rats. Total antioxidant, catalase, and malondialdehyde levels were assayed by standard procedures. Levels of AT1 receptor labeling, in renal and hepatic tissues of the three rat groups, were immunohistochemically investigated using an anti-AT1 receptor antibody. Levels of total antioxidant and catalase were significantly reduced, whereas malondialdehyde levels and AT1 receptor labeling were significantly increased in renal and hepatic tissues of diabetic control rats compared to normal rats. Compared to diabetic control rats, total antioxidant and catalase levels were significantly increased, whereas malondialdehyde levels and AT1 receptor labeling in the green-tea-treated diabetic group were significantly reduced throughout hepatic lobules and renal cortical and medullary vascular and tubular segments to levels comparable to those observed in normal rats. The capacity of green tea to modulate diabetes-induced oxidative stress and AT1 receptor upregulation may be beneficial in opposing the deleterious effects of excessive angiotensin II signaling, manifested by progressive renal and hepatic tissue damage.