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Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats

This study investigates the potential of green tea to modulate oxidative stress and angiotensin II AT(1) 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...

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Autores principales: Thomson, Martha, Al-Qattan, Khaled, Mansour, Mohamed H., Ali, Muslim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518821/
https://www.ncbi.nlm.nih.gov/pubmed/23243444
http://dx.doi.org/10.1155/2012/409047
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author Thomson, Martha
Al-Qattan, Khaled
Mansour, Mohamed H.
Ali, Muslim
author_facet Thomson, Martha
Al-Qattan, Khaled
Mansour, Mohamed H.
Ali, Muslim
author_sort Thomson, Martha
collection PubMed
description This study investigates the potential of green tea to modulate oxidative stress and angiotensin II AT(1) 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 AT(1) receptor labeling, in renal and hepatic tissues of the three rat groups, were immunohistochemically investigated using an anti-AT(1) receptor antibody. Levels of total antioxidant and catalase were significantly reduced, whereas malondialdehyde levels and AT(1) 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 AT(1) 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 AT(1) receptor upregulation may be beneficial in opposing the deleterious effects of excessive angiotensin II signaling, manifested by progressive renal and hepatic tissue damage.
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spelling pubmed-35188212012-12-14 Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats Thomson, Martha Al-Qattan, Khaled Mansour, Mohamed H. Ali, Muslim Evid Based Complement Alternat Med Research Article This study investigates the potential of green tea to modulate oxidative stress and angiotensin II AT(1) 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 AT(1) receptor labeling, in renal and hepatic tissues of the three rat groups, were immunohistochemically investigated using an anti-AT(1) receptor antibody. Levels of total antioxidant and catalase were significantly reduced, whereas malondialdehyde levels and AT(1) 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 AT(1) 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 AT(1) receptor upregulation may be beneficial in opposing the deleterious effects of excessive angiotensin II signaling, manifested by progressive renal and hepatic tissue damage. Hindawi Publishing Corporation 2012 2012-11-14 /pmc/articles/PMC3518821/ /pubmed/23243444 http://dx.doi.org/10.1155/2012/409047 Text en Copyright © 2012 Martha Thomson et al. https://creativecommons.org/licenses/by/3.0/ 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.
spellingShingle Research Article
Thomson, Martha
Al-Qattan, Khaled
Mansour, Mohamed H.
Ali, Muslim
Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title_full Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title_fullStr Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title_full_unstemmed Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title_short Green Tea Attenuates Oxidative Stress and Downregulates the Expression of Angiotensin II AT(1) Receptor in Renal and Hepatic Tissues of Streptozotocin-Induced Diabetic Rats
title_sort green tea attenuates oxidative stress and downregulates the expression of angiotensin ii at(1) receptor in renal and hepatic tissues of streptozotocin-induced diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518821/
https://www.ncbi.nlm.nih.gov/pubmed/23243444
http://dx.doi.org/10.1155/2012/409047
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