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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 |
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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. 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.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2017/3764370</identifier><identifier>PMID: 28421194</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>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</subject><ispartof>BioMed research international, 2017-01, Vol.2017 (2017), p.1-13</ispartof><rights>Copyright © 2017 Bin Wu et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Bin Wu et al. 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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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DHM may have a great therapeutic potential in the treatment of DCM.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Bioflavonoids</subject><subject>Biomarkers - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular disease</subject><subject>Causes of</subject><subject>Cell growth</subject><subject>Complications and side effects</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetic Cardiomyopathies - etiology</subject><subject>Diabetic Cardiomyopathies - metabolism</subject><subject>Diabetic Cardiomyopathies - pathology</subject><subject>Diabetic Cardiomyopathies - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yi, Fu</au><au>Yuan, Ming</au><au>Guo, Tao</au><au>Fan, Miaomiao</au><au>Han, Dong</au><au>Luo, Jian</au><au>Lin, Jie</au><au>Wu, Bin</au><au>Tao, Ling</au><au>Montecucco, Fabrizio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dihydromyricetin Protects against Diabetic Cardiomyopathy in Streptozotocin-Induced Diabetic Mice</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>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.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>28421194</pmid><doi>10.1155/2017/3764370</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-0545-3338</orcidid><orcidid>https://orcid.org/0000-0002-5500-838X</orcidid><orcidid>https://orcid.org/0000-0002-0150-0264</orcidid><orcidid>https://orcid.org/0000-0002-7076-1185</orcidid><orcidid>https://orcid.org/0000-0003-0098-4137</orcidid><orcidid>https://orcid.org/0000-0002-8343-2567</orcidid><oa>free_for_read</oa></addata></record> |
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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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