The Effects of Diabetes Induction on the Rat Heart: Differences in Oxidative Stress, Inflammatory Cells, and Fibrosis between Subendocardial and Interstitial Myocardial Areas
Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. M...
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| description | Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. Male Wistar rats were allocated to 2 groups of 9 animals, a control (CT) group and streptozotocin-induced diabetes (DM). After 8 weeks, echocardiography morphometry, protein expression, and confocal microscopy in SEN and INT areas of the left ventricle (LV) were performed. The echocardiographic analysis showed that diabetes induction leads to cardiac dilation, hypertrophy, and LV diastolic dysfunction. As compared to CT, the induction of diabetes increased inflammatory cells and fibrosis in both SEN and INT areas of DM myocardium and increased ROS generation only in SEN. Comparing the SEN and INT areas in the DM group, inflammatory cells and fibrosis in SEN were greater than in INT. In conclusion, diabetic myocardium SEN area, wherein oxidative stress was more pronounced, is more susceptible to cardiac dysfunction than INT area. This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction. |
| doi_str_mv | 10.1155/2017/5343972 |
| format | Article |
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C. ; Tavares de Melo, Marcelo D. ; Tavares, Elaine R. ; Marques, Alyne F. ; Guido, Maria C. ; Maranhão, Raul Cavalcante</creator><contributor>Sobenin, Igor A.</contributor><creatorcontrib>Salemi, Vera M. C. ; Tavares de Melo, Marcelo D. ; Tavares, Elaine R. ; Marques, Alyne F. ; Guido, Maria C. ; Maranhão, Raul Cavalcante ; Sobenin, Igor A.</creatorcontrib><description>Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. Male Wistar rats were allocated to 2 groups of 9 animals, a control (CT) group and streptozotocin-induced diabetes (DM). After 8 weeks, echocardiography morphometry, protein expression, and confocal microscopy in SEN and INT areas of the left ventricle (LV) were performed. The echocardiographic analysis showed that diabetes induction leads to cardiac dilation, hypertrophy, and LV diastolic dysfunction. As compared to CT, the induction of diabetes increased inflammatory cells and fibrosis in both SEN and INT areas of DM myocardium and increased ROS generation only in SEN. Comparing the SEN and INT areas in the DM group, inflammatory cells and fibrosis in SEN were greater than in INT. In conclusion, diabetic myocardium SEN area, wherein oxidative stress was more pronounced, is more susceptible to cardiac dysfunction than INT area. This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2017/5343972</identifier><identifier>PMID: 28781721</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Blotting, Western ; Cardiomyopathy ; Collagen ; Cytokines ; Diabetes ; Diabetes Mellitus - immunology ; Diabetes Mellitus - metabolism ; Diabetes Mellitus - pathology ; Diabetes Mellitus, Experimental - immunology ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetic Cardiomyopathies - immunology ; Diabetic Cardiomyopathies - metabolism ; Echocardiography ; Fibrosis ; Gangrene ; Health aspects ; Heart - physiology ; Heart failure ; Heart muscle ; Inflammation ; Insulin ; Male ; Medical research ; Myocardium - immunology ; Myocardium - metabolism ; Myocardium - pathology ; Oxidative stress ; Oxidative Stress - physiology ; Rats ; Rats, Wistar ; Reactive Oxygen Species - metabolism ; Rodents ; Streptozocin ; Studies ; Tumor necrosis factor-TNF ; Ventricular Dysfunction, Left - immunology ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - pathology</subject><ispartof>Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-11</ispartof><rights>Copyright © 2017 Maria C. Guido et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Maria C. Guido et al. 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.</rights><rights>Copyright © 2017 Maria C. Guido et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-45fb30698ca39dd9eca8f8d667aebfc02ad45808ea1fa417b8ec767cafea07c43</citedby><cites>FETCH-LOGICAL-c499t-45fb30698ca39dd9eca8f8d667aebfc02ad45808ea1fa417b8ec767cafea07c43</cites><orcidid>0000-0003-1520-4914</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525092/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5525092/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28781721$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sobenin, Igor A.</contributor><creatorcontrib>Salemi, Vera M. 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This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cardiomyopathy</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - immunology</subject><subject>Diabetes Mellitus - metabolism</subject><subject>Diabetes Mellitus - pathology</subject><subject>Diabetes Mellitus, Experimental - immunology</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetic Cardiomyopathies - immunology</subject><subject>Diabetic Cardiomyopathies - metabolism</subject><subject>Echocardiography</subject><subject>Fibrosis</subject><subject>Gangrene</subject><subject>Health aspects</subject><subject>Heart - physiology</subject><subject>Heart failure</subject><subject>Heart muscle</subject><subject>Inflammation</subject><subject>Insulin</subject><subject>Male</subject><subject>Medical research</subject><subject>Myocardium - immunology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rodents</subject><subject>Streptozocin</subject><subject>Studies</subject><subject>Tumor necrosis factor-TNF</subject><subject>Ventricular Dysfunction, Left - immunology</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - pathology</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkt9rFDEQxxdRbK2--SwBXwR7Nslu9ocPwnG29qBSsPU5zCaTNmUvqUm29f4p_0az3nlVnySBhMlnvjMTvkXxktF3jAlxxClrjkRZlV3DHxX7rKv4jHZd9Xh3p3SveBbjDaV1ySv2tNjjbdOyhrP94sflNZJjY1ClSLwhHy30mDCSpdOjStY7knfK0BdI5BQhpPcZygkBncqcdeT8u9WQ7B2SixQwxsOcbAZYrSD5sCYLHIYcA6fJie2DjzaSXOMe0ZGLsUenvYKgLQy_mKVLGGKyaQp8Xu_e5gEhPi-eGBgivtieB8XXk-PLxens7PzTcjE_m6mq69KsEqYvad21CspO6w4VtKbVdd0A9kZRDroSLW0RmIGKNX2LqqkbBQaBNqoqD4oPG93bsV-hVuhSgEHeBruCsJYerPz7xdlreeXvpBBc0I5ngTdbgeC_jRiTXNmo8k-AQz9GyTqe26NMTOjrf9AbPwaXx5so3maE0gfqCgaU1hmf66pJVM6FEK2gNReZOtxQKv9zDGh2LTMqJ7vIyS5ya5eMv_pzzB382x8ZeLsBrq3TcG__Uw4zgwYe6OzEvMqfmY7UPA</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Salemi, Vera M. 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C.</au><au>Tavares de Melo, Marcelo D.</au><au>Tavares, Elaine R.</au><au>Marques, Alyne F.</au><au>Guido, Maria C.</au><au>Maranhão, Raul Cavalcante</au><au>Sobenin, Igor A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effects of Diabetes Induction on the Rat Heart: Differences in Oxidative Stress, Inflammatory Cells, and Fibrosis between Subendocardial and Interstitial Myocardial Areas</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Diabetic cardiomyopathy (DCM) is characterized by cardiac remodeling and impaired diastolic function that may lead to heart failure. The aim of this study was to evaluate oxidative stress, inflammatory cells, and fibrosis in both subendocardial (SEN) and interstitial (INT) areas of the myocardium. Male Wistar rats were allocated to 2 groups of 9 animals, a control (CT) group and streptozotocin-induced diabetes (DM). After 8 weeks, echocardiography morphometry, protein expression, and confocal microscopy in SEN and INT areas of the left ventricle (LV) were performed. The echocardiographic analysis showed that diabetes induction leads to cardiac dilation, hypertrophy, and LV diastolic dysfunction. As compared to CT, the induction of diabetes increased inflammatory cells and fibrosis in both SEN and INT areas of DM myocardium and increased ROS generation only in SEN. Comparing the SEN and INT areas in the DM group, inflammatory cells and fibrosis in SEN were greater than in INT. In conclusion, diabetic myocardium SEN area, wherein oxidative stress was more pronounced, is more susceptible to cardiac dysfunction than INT area. This finding can be important for the understanding of the heart remodeling process occurring in DCM and perhaps to engender targeted therapies to attenuate or revert DCM-related diastolic dysfunction.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>28781721</pmid><doi>10.1155/2017/5343972</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-1520-4914</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Blotting, Western Cardiomyopathy Collagen Cytokines Diabetes Diabetes Mellitus - immunology Diabetes Mellitus - metabolism Diabetes Mellitus - pathology Diabetes Mellitus, Experimental - immunology Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic Cardiomyopathies - immunology Diabetic Cardiomyopathies - metabolism Echocardiography Fibrosis Gangrene Health aspects Heart - physiology Heart failure Heart muscle Inflammation Insulin Male Medical research Myocardium - immunology Myocardium - metabolism Myocardium - pathology Oxidative stress Oxidative Stress - physiology Rats Rats, Wistar Reactive Oxygen Species - metabolism Rodents Streptozocin Studies Tumor necrosis factor-TNF Ventricular Dysfunction, Left - immunology Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - pathology |
| title | The Effects of Diabetes Induction on the Rat Heart: Differences in Oxidative Stress, Inflammatory Cells, and Fibrosis between Subendocardial and Interstitial Myocardial Areas |
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