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Dihydromyricetin Protects against Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetic Mice

Diabetic cardiomyopathy (DCM) is an important cause of heart failure in diabetic patients. The present study sought to explore the potential effects of dihydromyricetin (DHM) on DCM and its possible mechanism. A diabetic model was induced by intraperitoneal injection of streptozotocin (STZ) in C57BL...

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Published in:BioMed research international 2017-01, Vol.2017 (2017), p.1-13
Main Authors: Yi, Fu, Yuan, Ming, Guo, Tao, Fan, Miaomiao, Han, Dong, Luo, Jian, Lin, Jie, Wu, Bin, Tao, Ling
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cited_by cdi_FETCH-LOGICAL-c598t-130bf67601e0cc3cf797458c0eebd1aad55d40866e11bc7dd9aa3989150b92d23
cites cdi_FETCH-LOGICAL-c598t-130bf67601e0cc3cf797458c0eebd1aad55d40866e11bc7dd9aa3989150b92d23
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container_title BioMed research international
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creator Yi, Fu
Yuan, Ming
Guo, Tao
Fan, Miaomiao
Han, Dong
Luo, Jian
Lin, Jie
Wu, Bin
Tao, Ling
description Diabetic cardiomyopathy (DCM) is an important cause of heart failure in diabetic patients. The present study sought to explore the potential effects of dihydromyricetin (DHM) on DCM and its possible mechanism. A diabetic model was induced by intraperitoneal injection of streptozotocin (STZ) in C57BL/6J mice. Two weeks after the STZ injection, mice were randomly allocated into the following 4 groups for treatment: the control group (CON), the control treated with DHM group (CON + DHM), the diabetes group (DM), and the diabetes treated with DHM group (DM + DHM). DHM was dissolved in distilled water and administered daily by gavage. For 14 weeks, the CON + DHM group and DM + DHM group were given a dose of 100 mg/kg/day DHM (Sigma-Aldrich), while the CON and DM groups were intragastrically given equivalent volumes of distilled water. Assessments and comparisons were made among the groups based on cardiac function and structural changes, inflammation factors, markers of oxidative stress, mitochondria function, apoptosis, and autophagy. The DHM treatment normalized body weight, preserved cardiac function, attenuated oxidative stress (MDA, SOD, and GSH-Px), reduced the levels of inflammation factors (IL-6, TNF-α), alleviated pathological changes, improved mitochondrial function (ATP content, CS activity, and complex Ι/ΙΙ/ΙΙΙ/ΙV/V activities), inhibited cardiac apoptosis, and restored autophagy in diabetic mice. DHM may have a great therapeutic potential in the treatment of DCM.
doi_str_mv 10.1155/2017/3764370
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The present study sought to explore the potential effects of dihydromyricetin (DHM) on DCM and its possible mechanism. A diabetic model was induced by intraperitoneal injection of streptozotocin (STZ) in C57BL/6J mice. Two weeks after the STZ injection, mice were randomly allocated into the following 4 groups for treatment: the control group (CON), the control treated with DHM group (CON + DHM), the diabetes group (DM), and the diabetes treated with DHM group (DM + DHM). DHM was dissolved in distilled water and administered daily by gavage. For 14 weeks, the CON + DHM group and DM + DHM group were given a dose of 100 mg/kg/day DHM (Sigma-Aldrich), while the CON and DM groups were intragastrically given equivalent volumes of distilled water. Assessments and comparisons were made among the groups based on cardiac function and structural changes, inflammation factors, markers of oxidative stress, mitochondria function, apoptosis, and autophagy. 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source Wiley-Blackwell Open Access Collection; Publicly Available Content Database
subjects Animals
Antioxidants
Apoptosis
Apoptosis - drug effects
Autophagy
Autophagy - drug effects
Bioflavonoids
Biomarkers - metabolism
Cardiomyocytes
Cardiomyopathy
Cardiovascular disease
Causes of
Cell growth
Complications and side effects
Cytokines
Diabetes
Diabetes Mellitus, Experimental - drug therapy
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Experimental - pathology
Diabetic Cardiomyopathies - etiology
Diabetic Cardiomyopathies - metabolism
Diabetic Cardiomyopathies - pathology
Diabetic Cardiomyopathies - prevention & control
Flavones
Flavonoids
Flavonols - pharmacology
Gangrene
Health aspects
Heart diseases
Heart failure
Inflammation - drug therapy
Inflammation - metabolism
Inflammation - pathology
Insulin resistance
Laboratory animals
Male
Metabolic disorders
Mice
Musculoskeletal system
Oxidative stress
Oxidative Stress - drug effects
Phosphorylation
Prevention
Proteins
Rodents
Streptozocin
Tumor necrosis factor-TNF
title Dihydromyricetin Protects against Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetic Mice
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