کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11007588 | 1540606 | 2018 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fisetin inhibits cardiac hypertrophy by suppressing oxidative stress
ترجمه فارسی عنوان
فیستئون با سرکوب استرس اکسیداتیو، مانع هیپرتروفی قلبی می شود
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کلمات کلیدی
Heme oxygenase-1LVPWdLVESDLVEDdSOD1HO-1NACCATANPERK1/2 - ERK1 / 2JNK1/2 - JNK1 / 2MAPK - MAPKN-acetylcysteine - N-استیل سیستئینROS - ROSLeft ventricular end-diastolic dimension - ابعاد انتهایی دیاستولیک بطن چپAortic banding - باندینگ آئورتLeft ventricular end-systolic dimension - بعد سیستولیک پایین بطن چپOxidative stress - تنش اکسیداتیوsuperoxide dismutase 1 - سوپر اکسید دیسموتاز 1phenylephrine - فنیل آفرینFisetin - فیستینheart failure - نارسایی قلبیCardiac hypertrophy - هیپرتروفی قلبیextracellular signal-regulated protein kinase 1/2 - پروتئین کیناز 1/2 تنظیم شده توسط سیگنال خارج سلولیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenatrial natriuretic peptide - پپتید نایروئیدوری دهلیزCatalase - کاتالازejection fraction - کسری خروجیfractional shortening - کوتاه کردن کسریReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Cardiac hypertrophy is a pathophysiological response to various pathological stresses and ultimately leads to heart failure. Oxidative stress is one of the critical processes involved in hypertrophy development. Fisetin, a small molecular flavonoid, has been shown to have anti-oxidative, anti-proliferative and anti-inflammatory properties. However, the effect of fisetin on cardiac hypertrophy remains unknown. In our present study, we showed that fisetin inhibited pressure overload-induced cardiac hypertrophy, improved cardiac function in vivo and suppressed phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. Reactive oxygen species (ROS) levels were markedly decreased by fisetin treatment in both hypertrophic hearts and cardiomyocytes. Moreover, fisetin significantly up-regulated the expression of antioxidative genes, including catalase (CAT), superoxide dismutase 1 (SOD1) and heme oxygenase 1 (HO-1). Furthermore, co-treatment with N-acetylcysteine (NAC; ROS scavenger) and fisetin did not have synergistic inhibitory effects on PE-induced cardiomyocyte hypertrophy, indicating that the anti-hypertrophic effects of fisetin are mainly associated with the blockade of oxidative stress. Finally, the pro-hypertrophic signaling pathways, mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) kinase, were found to be suppressed by fisetin after pressure overload and PE treatment. In conclusion, our study revealed that fisetin protects against cardiac hypertrophy and that oxidative stress inhibition may be one of the pivotal mechanisms involved.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 62, December 2018, Pages 221-229
Journal: The Journal of Nutritional Biochemistry - Volume 62, December 2018, Pages 221-229
نویسندگان
Bin Dong, Chen Liu, Ruicong Xue, Yan Wang, Yu Sun, Zhuomin Liang, Wendong Fan, Jingzhou Jiang, Jingjing Zhao, Qiao Su, Gang Dai, Yugang Dong, Huiling Huang,