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Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats

BACKGROUND: Increasing studies have shown that dyslipidemia and inflammatory responses play important roles in the progression of microvascular diabetic complications. Esculin (ES), a coumarin derivative, was extracted from Fraxinus rhynchophylla. The present study was to evaluate the potential effe...

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Autores principales: Wang, Yue-Hua, Liu, Yan-Hong, He, Guo-Rong, Lv, Yang, Du, Guan-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640113/
https://www.ncbi.nlm.nih.gov/pubmed/26552745
http://dx.doi.org/10.1186/s12906-015-0817-y
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author Wang, Yue-Hua
Liu, Yan-Hong
He, Guo-Rong
Lv, Yang
Du, Guan-Hua
author_facet Wang, Yue-Hua
Liu, Yan-Hong
He, Guo-Rong
Lv, Yang
Du, Guan-Hua
author_sort Wang, Yue-Hua
collection PubMed
description BACKGROUND: Increasing studies have shown that dyslipidemia and inflammatory responses play important roles in the progression of microvascular diabetic complications. Esculin (ES), a coumarin derivative, was extracted from Fraxinus rhynchophylla. The present study was to evaluate the potential effects of ES on lipid metabolism, inflammation responses and renal damage in streptozotocin (STZ)-induced experimental diabetic rats and explore the possible mechanism. METHODS: Diabetic rat model was established by administration high-glucose-fat diet and intraperitoneal injection of STZ 45 mg/kg. ES was administrated to diabetic rats intragastrically at 10, 30 and 90 mg/kg for 10 weeks respectively. The levels of triglycerides (TG), total cholesterol (T-CHO), low density lipoproteins (LDL), and high-density-cholesterol (HDL-C) in serum were measured. IL-1, IL-6, ICAM-1, NO, NAGL, and AGEs level in serum were detected by ELISA assay. The accumulation of AGEs in kidney tissue was examined by immunohistochemistry assay. RESULTS: The results showed that ES could decrease TG, T-CHO, LDL levels in serum of diabetic rats in a dose dependent manner. ES also decreased IL-1, IL-6, ICAM-1, NO and NGAL levels in serum of diabetic rats in a dose dependent manner. Furthermore, ES at 30 and 90 mg/kg significantly decreased AGEs level in serum and alleviated AGEs accumulation in renal in diabetic rats. CONCLUSIONS: Our findings indicate that ES could improve dyslipidemia, inflammation responses, renal damage in STZ-induced diabetic rats and the possible mechanism might be associated with the inhibition of AGEs formation.
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spelling pubmed-46401132015-11-11 Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats Wang, Yue-Hua Liu, Yan-Hong He, Guo-Rong Lv, Yang Du, Guan-Hua BMC Complement Altern Med Research Article BACKGROUND: Increasing studies have shown that dyslipidemia and inflammatory responses play important roles in the progression of microvascular diabetic complications. Esculin (ES), a coumarin derivative, was extracted from Fraxinus rhynchophylla. The present study was to evaluate the potential effects of ES on lipid metabolism, inflammation responses and renal damage in streptozotocin (STZ)-induced experimental diabetic rats and explore the possible mechanism. METHODS: Diabetic rat model was established by administration high-glucose-fat diet and intraperitoneal injection of STZ 45 mg/kg. ES was administrated to diabetic rats intragastrically at 10, 30 and 90 mg/kg for 10 weeks respectively. The levels of triglycerides (TG), total cholesterol (T-CHO), low density lipoproteins (LDL), and high-density-cholesterol (HDL-C) in serum were measured. IL-1, IL-6, ICAM-1, NO, NAGL, and AGEs level in serum were detected by ELISA assay. The accumulation of AGEs in kidney tissue was examined by immunohistochemistry assay. RESULTS: The results showed that ES could decrease TG, T-CHO, LDL levels in serum of diabetic rats in a dose dependent manner. ES also decreased IL-1, IL-6, ICAM-1, NO and NGAL levels in serum of diabetic rats in a dose dependent manner. Furthermore, ES at 30 and 90 mg/kg significantly decreased AGEs level in serum and alleviated AGEs accumulation in renal in diabetic rats. CONCLUSIONS: Our findings indicate that ES could improve dyslipidemia, inflammation responses, renal damage in STZ-induced diabetic rats and the possible mechanism might be associated with the inhibition of AGEs formation. BioMed Central 2015-11-09 /pmc/articles/PMC4640113/ /pubmed/26552745 http://dx.doi.org/10.1186/s12906-015-0817-y Text en © Wang et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Wang, Yue-Hua
Liu, Yan-Hong
He, Guo-Rong
Lv, Yang
Du, Guan-Hua
Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title_full Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title_fullStr Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title_full_unstemmed Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title_short Esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
title_sort esculin improves dyslipidemia, inflammation and renal damage in streptozotocin-induced diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640113/
https://www.ncbi.nlm.nih.gov/pubmed/26552745
http://dx.doi.org/10.1186/s12906-015-0817-y
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