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Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats

Traditional Chinese medication has been utilized by Chinese medical practitioners to treat the varied symptoms of diabetes mellitus (DM). Notably, guava leaf has been used to treat diabetes in Asia. Our present study has been designed to analyze the action of guava leaf extract (GLE) at the molecula...

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Autores principales: Jayachandran, Muthukumaran, Vinayagam, Ramachandran, Ambati, Ranga Rao, Xu, Baojun, Chung, Stephen Sum Man
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835305/
https://www.ncbi.nlm.nih.gov/pubmed/29670899
http://dx.doi.org/10.1155/2018/4601649
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author Jayachandran, Muthukumaran
Vinayagam, Ramachandran
Ambati, Ranga Rao
Xu, Baojun
Chung, Stephen Sum Man
author_facet Jayachandran, Muthukumaran
Vinayagam, Ramachandran
Ambati, Ranga Rao
Xu, Baojun
Chung, Stephen Sum Man
author_sort Jayachandran, Muthukumaran
collection PubMed
description Traditional Chinese medication has been utilized by Chinese medical practitioners to treat the varied symptoms of diabetes mellitus (DM). Notably, guava leaf has been used to treat diabetes in Asia. Our present study has been designed to analyze the action of guava leaf extract (GLE) at the molecular level in treating DM. A low dose of streptozotocin (STZ) was used to induce experimental diabetes in animals. Rats were treated with GLE at different concentrations (100, 200, and 400 mg/kg b.w.). The standard drug glibenclamide (GB) (600 μg/kg b.w.) was used for comparison. The diabetic rats showed a reduced level of insulin, accompanied by exaggerated levels of blood glucose, lipid peroxidation product, and augmented expressions of inflammatory cytokines, and showed reduced levels of antioxidants compared to the control rats. Supplementation with GLE counteracted the consequences of STZ. It suppresses the oxidative stress and inhibits the state of inflammation and the results are almost similar to that of standard drug group (GB group 5). Our present research, therefore, provides useful data concerning guava leaf extract by a thorough assessment in diabetes management. Being a natural product, additional analysis on GLE can shed light on finding effective phytochemicals within the field of diabetes mellitus.
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spelling pubmed-58353052018-04-18 Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats Jayachandran, Muthukumaran Vinayagam, Ramachandran Ambati, Ranga Rao Xu, Baojun Chung, Stephen Sum Man Biomed Res Int Research Article Traditional Chinese medication has been utilized by Chinese medical practitioners to treat the varied symptoms of diabetes mellitus (DM). Notably, guava leaf has been used to treat diabetes in Asia. Our present study has been designed to analyze the action of guava leaf extract (GLE) at the molecular level in treating DM. A low dose of streptozotocin (STZ) was used to induce experimental diabetes in animals. Rats were treated with GLE at different concentrations (100, 200, and 400 mg/kg b.w.). The standard drug glibenclamide (GB) (600 μg/kg b.w.) was used for comparison. The diabetic rats showed a reduced level of insulin, accompanied by exaggerated levels of blood glucose, lipid peroxidation product, and augmented expressions of inflammatory cytokines, and showed reduced levels of antioxidants compared to the control rats. Supplementation with GLE counteracted the consequences of STZ. It suppresses the oxidative stress and inhibits the state of inflammation and the results are almost similar to that of standard drug group (GB group 5). Our present research, therefore, provides useful data concerning guava leaf extract by a thorough assessment in diabetes management. Being a natural product, additional analysis on GLE can shed light on finding effective phytochemicals within the field of diabetes mellitus. Hindawi 2018-02-18 /pmc/articles/PMC5835305/ /pubmed/29670899 http://dx.doi.org/10.1155/2018/4601649 Text en Copyright © 2018 Muthukumaran Jayachandran et al. https://creativecommons.org/licenses/by/4.0/ 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
Jayachandran, Muthukumaran
Vinayagam, Ramachandran
Ambati, Ranga Rao
Xu, Baojun
Chung, Stephen Sum Man
Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title_full Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title_fullStr Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title_full_unstemmed Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title_short Guava Leaf Extract Diminishes Hyperglycemia and Oxidative Stress, Prevents β-Cell Death, Inhibits Inflammation, and Regulates NF-kB Signaling Pathway in STZ Induced Diabetic Rats
title_sort guava leaf extract diminishes hyperglycemia and oxidative stress, prevents β-cell death, inhibits inflammation, and regulates nf-kb signaling pathway in stz induced diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835305/
https://www.ncbi.nlm.nih.gov/pubmed/29670899
http://dx.doi.org/10.1155/2018/4601649
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