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Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats
PURPOSE: Advanced glycation end products (AGE) are associated in the development of several pathophysiologies including diabetic cataract. Earlier we have reported that some common dietary agents have antiglycating activity and ginger (Zingiber officinalis) was one of the few prominent agents that e...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Molecular Vision
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925903/ https://www.ncbi.nlm.nih.gov/pubmed/20806076 |
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author | Saraswat, Megha Suryanarayana, Palla Reddy, Paduru Yadagiri Patil, Madhoosudan A. Balakrishna, Nagalla Reddy, Geereddy Bhanuprakash |
author_facet | Saraswat, Megha Suryanarayana, Palla Reddy, Paduru Yadagiri Patil, Madhoosudan A. Balakrishna, Nagalla Reddy, Geereddy Bhanuprakash |
author_sort | Saraswat, Megha |
collection | PubMed |
description | PURPOSE: Advanced glycation end products (AGE) are associated in the development of several pathophysiologies including diabetic cataract. Earlier we have reported that some common dietary agents have antiglycating activity and ginger (Zingiber officinalis) was one of the few prominent agents that effectively prevented AGE formation in vitro. In this study we investigated the potential of ginger to prevent diabetic cataract in rats. METHODS: Diabetes was induced in Wistar-NIN rats by intraperitoneal injection of streptozotocin (35 mg/kg bodyweight) and the control rats received vehicle alone. While a set of diabetic animals received AIN-93 diet, another set received either 0.5 or 3% ginger in their diet for a period of two months. Cataract progression was monitored by slit-lamp biomicroscope. At the end of two months, the animals were sacrificed to evaluate non-enzymatic glycation and osmotic stress in the eye lens. RESULTS: Slit-lamp examination revealed that feeding of ginger not only delayed the onset but also the progression of cataract in rats. Molecular analyses indicated that feeding of ginger significantly inhibited the formation of various AGE products including carboxymethyl lysine in the eye lens. In addition, ginger also countered hyperglycemia-induced osmotic stress in the lens. CONCLUSIONS: The results indicated that ginger was effective against the development of diabetic cataract in rats mainly through its antiglycating potential and to a lesser extent by inhibition of the polyol pathway. Thus, ingredients of dietary sources, such as ginger, may be explored for the prevention or delay of diabetic complications. |
format | Text |
id | pubmed-2925903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Molecular Vision |
record_format | MEDLINE/PubMed |
spelling | pubmed-29259032010-08-30 Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats Saraswat, Megha Suryanarayana, Palla Reddy, Paduru Yadagiri Patil, Madhoosudan A. Balakrishna, Nagalla Reddy, Geereddy Bhanuprakash Mol Vis Research Article PURPOSE: Advanced glycation end products (AGE) are associated in the development of several pathophysiologies including diabetic cataract. Earlier we have reported that some common dietary agents have antiglycating activity and ginger (Zingiber officinalis) was one of the few prominent agents that effectively prevented AGE formation in vitro. In this study we investigated the potential of ginger to prevent diabetic cataract in rats. METHODS: Diabetes was induced in Wistar-NIN rats by intraperitoneal injection of streptozotocin (35 mg/kg bodyweight) and the control rats received vehicle alone. While a set of diabetic animals received AIN-93 diet, another set received either 0.5 or 3% ginger in their diet for a period of two months. Cataract progression was monitored by slit-lamp biomicroscope. At the end of two months, the animals were sacrificed to evaluate non-enzymatic glycation and osmotic stress in the eye lens. RESULTS: Slit-lamp examination revealed that feeding of ginger not only delayed the onset but also the progression of cataract in rats. Molecular analyses indicated that feeding of ginger significantly inhibited the formation of various AGE products including carboxymethyl lysine in the eye lens. In addition, ginger also countered hyperglycemia-induced osmotic stress in the lens. CONCLUSIONS: The results indicated that ginger was effective against the development of diabetic cataract in rats mainly through its antiglycating potential and to a lesser extent by inhibition of the polyol pathway. Thus, ingredients of dietary sources, such as ginger, may be explored for the prevention or delay of diabetic complications. Molecular Vision 2010-08-10 /pmc/articles/PMC2925903/ /pubmed/20806076 Text en Copyright © 2010 Molecular Vision. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of 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 Saraswat, Megha Suryanarayana, Palla Reddy, Paduru Yadagiri Patil, Madhoosudan A. Balakrishna, Nagalla Reddy, Geereddy Bhanuprakash Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title | Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title_full | Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title_fullStr | Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title_full_unstemmed | Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title_short | Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats |
title_sort | antiglycating potential of zingiber officinalis and delay of diabetic cataract in rats |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925903/ https://www.ncbi.nlm.nih.gov/pubmed/20806076 |
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