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Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats

Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats. Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg(−1) body weight (BW)). Galangin (8 mg kg(−1) BW) or glibenclami...

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Autores principales: Aloud, Amal A., Veeramani, Chinnadurai, Govindasamy, Chandramohan, Alsaif, Mohammed A., Al-Numair, Khalid S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748697/
https://www.ncbi.nlm.nih.gov/pubmed/28813209
http://dx.doi.org/10.1080/13510002.2017.1365224
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author Aloud, Amal A.
Veeramani, Chinnadurai
Govindasamy, Chandramohan
Alsaif, Mohammed A.
Al-Numair, Khalid S.
author_facet Aloud, Amal A.
Veeramani, Chinnadurai
Govindasamy, Chandramohan
Alsaif, Mohammed A.
Al-Numair, Khalid S.
author_sort Aloud, Amal A.
collection PubMed
description Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats. Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg(−1) body weight (BW)). Galangin (8 mg kg(−1) BW) or glibenclamide (600 µg kg(−1) BW) was given orally daily once for 45 days to both healthy and diabetic rats. Results: Diabetic rats showed significant (P < 0.05) increase in liver mitochondrial oxidant [Thiobarbituric acid reactive substance (TBARS)] level and a significant decrease in enzymatic [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and non-enzymatic (reduced glutathione (GSH)) antioxidant levels when compared with healthy rats. The mitochondrial enzymes isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) and mitochondrial respiratory chain enzymes NADH-dehydrogenase and Cytochrome c-oxidase were decreased significantly (P < 0.05) in diabetic rats when compared with healthy rats. A natural flavonoid galangin administered to hyperglycemia-induced rats resulted in the following findings as compared to hyperglycemia-induced control rats: the oxidant levels decreased significantly (P < 0.05); the enzymatic and non-enzymatic antioxidant levels increased significantly (P < 0.05) and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (P < 0.05). Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats.
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spelling pubmed-67486972020-04-15 Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats Aloud, Amal A. Veeramani, Chinnadurai Govindasamy, Chandramohan Alsaif, Mohammed A. Al-Numair, Khalid S. Redox Rep Research Article Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats. Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg(−1) body weight (BW)). Galangin (8 mg kg(−1) BW) or glibenclamide (600 µg kg(−1) BW) was given orally daily once for 45 days to both healthy and diabetic rats. Results: Diabetic rats showed significant (P < 0.05) increase in liver mitochondrial oxidant [Thiobarbituric acid reactive substance (TBARS)] level and a significant decrease in enzymatic [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and non-enzymatic (reduced glutathione (GSH)) antioxidant levels when compared with healthy rats. The mitochondrial enzymes isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) and mitochondrial respiratory chain enzymes NADH-dehydrogenase and Cytochrome c-oxidase were decreased significantly (P < 0.05) in diabetic rats when compared with healthy rats. A natural flavonoid galangin administered to hyperglycemia-induced rats resulted in the following findings as compared to hyperglycemia-induced control rats: the oxidant levels decreased significantly (P < 0.05); the enzymatic and non-enzymatic antioxidant levels increased significantly (P < 0.05) and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (P < 0.05). Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats. Taylor & Francis 2017-08-16 /pmc/articles/PMC6748697/ /pubmed/28813209 http://dx.doi.org/10.1080/13510002.2017.1365224 Text en © 2017 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Aloud, Amal A.
Veeramani, Chinnadurai
Govindasamy, Chandramohan
Alsaif, Mohammed A.
Al-Numair, Khalid S.
Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title_full Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title_fullStr Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title_full_unstemmed Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title_short Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
title_sort galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748697/
https://www.ncbi.nlm.nih.gov/pubmed/28813209
http://dx.doi.org/10.1080/13510002.2017.1365224
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