Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus
المؤلفون المشاركون
Yang, Jian
Lu, Linhe
Ma, Jipeng
Sun, Mingming
Wang, Xiaowu
Gao, Erhe
Lu, Lintao
Yang, Lifang
Ren, Jun
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-01-09
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Diabetes mellitus, a worldwide health threat, is considered an independent risk factor for cardiovascular diseases.
The overall cardiovascular risk of diabetes is similar to the one having one myocardial infarction (MI) attack although the precise impact of diabetes on MI-induced myocardial anomalies remains elusive.
Given that mortality following MI is much greater in diabetic patients compared to nondiabetic patients, this study was designed to examine the effect of melatonin on MI injury-induced myocardial dysfunction in diabetes.
Adult mice were made diabetic using high-fat feeding and streptozotocin (100 mg/kg body weight) prior to MI and were treated with melatonin (50 mg/kg/d, p.o.) for 4 weeks prior to assessment of cardiac geometry and function.
The MI procedure in diabetes displayed overt changes in cardiac geometry (chamber dilation and interstitial fibrosis) and functional anomalies (reduced fractional shortening and cardiomyocyte contractile capacity) in association with elevated c-Jun N-terminal kinase (JNK) phosphorylation and p53 level.
Melatonin treatment markedly attenuated cardiac dysfunction and myocardial fibrosis in post-MI diabetic mice.
Furthermore, melatonin decreased JNK phosphorylation, reduced p53 levels, and suppressed apoptosis in hearts from the post-MI diabetic group.
In vitro findings revealed that melatonin effectively counteracted high-glucose/high fat-hypoxia-induced cardiomyocyte apoptosis and contractile dysfunction through a JNK-mediated mechanism, the effects of which were impaired by the JNK activator anisomycin.
In summary, our study suggests that melatonin protects against myocardial injury in post-MI mice with diabetes, which offers a new therapeutic strategy for the management of MI-induced cardiac injury in diabetes.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Lu, Linhe& Ma, Jipeng& Sun, Mingming& Wang, Xiaowu& Gao, Erhe& Lu, Lintao…[et al.]. 2020. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Lu, Linhe…[et al.]. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Lu, Linhe& Ma, Jipeng& Sun, Mingming& Wang, Xiaowu& Gao, Erhe& Lu, Lintao…[et al.]. Melatonin Ameliorates MI-Induced Cardiac Remodeling and Apoptosis through a JNKp53-Dependent Mechanism in Diabetes Mellitus. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1203750
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203750
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر