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Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6TAK1MAPK and Nrf2 Signaling Pathway
المؤلفون المشاركون
Liao, Hai-Han
Tang, Qi-Zhu
Deng, Wei
Feng, Hong
Zhang, Nan
Chen, Si
Meng, Yan-yan
Yang, Jing-jing
Li, Wen-jin
Wu, Hai-ming
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-12-06
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Myricetin (Myr) is a common plant-derived polyphenol and is well recognized for its multiple activities including antioxidant, anti-inflammation, anticancer, and antidiabetes.
Our previous studies indicated that Myr protected mouse heart from lipopolysaccharide and streptozocin-induced injuries.
However, it remained to be unclear whether Myr could prevent mouse heart from pressure overload-induced pathological hypertrophy.
Wild type (WT) and cardiac Nrf2 knockdown (Nrf2-KD) mice were subjected to aortic banding (AB) surgery and then administered with Myr (200 mg/kg/d) for 6 weeks.
Myr significantly alleviated AB-induced cardiac hypertrophy, fibrosis, and cardiac dysfunction in both WT and Nrf2-KD mice.
Myr also inhibited phenylephrine- (PE-) induced neonatal rat cardiomyocyte (NRCM) hypertrophy and hypertrophic markers’ expression in vitro.
Mechanically, Myr markedly increased Nrf2 activity, decreased NF-κB activity, and inhibited TAK1/p38/JNK1/2 MAPK signaling in WT mouse hearts.
We further demonstrated that Myr could inhibit TAK1/p38/JNK1/2 signaling via inhibiting Traf6 ubiquitination and its interaction with TAK1 after Nrf2 knockdown in NRCM.
These results strongly suggested that Myr could attenuate pressure overload-induced pathological hypertrophy in vivo and PE-induced NRCM hypertrophy via enhancing Nrf2 activity and inhibiting TAK1/P38/JNK1/2 phosphorylation by regulating Traf6 ubiquitination.
Thus, Myr might be a potential strategy for therapy or adjuvant therapy for malignant cardiac hypertrophy.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Liao, Hai-Han& Zhang, Nan& Meng, Yan-yan& Feng, Hong& Yang, Jing-jing& Li, Wen-jin…[et al.]. 2019. Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6TAK1MAPK and Nrf2 Signaling Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1204528
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Liao, Hai-Han…[et al.]. Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6TAK1MAPK and Nrf2 Signaling Pathway. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1204528
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Liao, Hai-Han& Zhang, Nan& Meng, Yan-yan& Feng, Hong& Yang, Jing-jing& Li, Wen-jin…[et al.]. Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6TAK1MAPK and Nrf2 Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1204528
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204528
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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