کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739543 | 1046879 | 2005 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Isorhapontigenin, a new resveratrol analog, attenuates cardiac hypertrophy via blocking signaling transduction pathways
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کلمات کلیدی
NF-κBJun NH2-terminal kinaseIsorhapontigeninPDTCphorbol 12-myristate 13-acetateAP-1p70S6KDCFH-DATACNACERKPI3KJnk2′,7′-dichlorofluorescein diacetate - 2 '، 7'-dichlorofluorescein diacetatePMA - LDC هاMAPK - MAPKN-acetylcysteine - N-استیل سیستئینROS - ROSAngiotensin II - آنژیوتانسین دوISO - ایزوAng II - دومpyrrolidine dithiocarbamate - دی اتیل کربامات پیرولیدینnuclear factor-κB - فاکتور هسته ای κBphosphoinositide-3-kinase - فسفونیوییدید-3-کینازactivator protein-1 - پروتئین فعال کننده-1mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
Cardiac hypertrophy is a major cause of morbidity and mortality worldwide. The hypertrophic process is mediated, in part, by oxidative stress-mediated signaling pathways. We hypothesized that isorhapontigenin (ISO), a new resveratrol analog, inhibits cardiac hypertrophy by blocking oxidative stress and oxidative stress-mediated signaling pathways. We treated cardiomyocytes with angiotensin II (Ang II) with or without ISO and found that ISO inhibited Ang II-induced cardiac hypertrophy. These effects were associated with a decrease in the levels of reactive oxygen species and H2O2 and the content of intracellular malonaldehyde and an increase in the activities of superoxide dismutase and glutathione peroxidase. Ang II induced the phosphorylation of PKC, Erk1/2, JNK, and p38 in cardiomyocytes and such phosphorylation was inhibited by ISO. ISO also blocked the PKC-dependent PI3K-Akt-GSK3β/p70S6K pathway. These effects lead to direct or indirect inhibition of NF-κB and AP-1 activation. Our results revealed that pretreatment with ISO significantly inhibited Ang II-mediated NF-κB through affecting the degradation and phosphorylation of IκBα and the activity of IKKβ and AP-1 activation by influencing the expression of c-Fos and c-Jun proteins. In addition, we also established the molecular link between activation of PKC and MAPKs and activation of NF-κB and AP-1 in cardiomyocytes. We also found that ISO treatment significantly attenuated heart weight/body weight ratio by approximately 25%, decreased posterior wall thickness and left ventricle diastolic and systolic diameters, and increased 10% fractional shortening in an aortic-banded rat model. Furthermore, treatment with ISO significantly decreased cardiac myocyte size and systolic blood pressure. These findings suggest that ISO prevents the development of cardiac hypertrophy through an antioxidant mechanism involving inhibition of different intracellular signaling transduction pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 38, Issue 2, 15 January 2005, Pages 243-257
Journal: Free Radical Biology and Medicine - Volume 38, Issue 2, 15 January 2005, Pages 243-257
نویسندگان
Hong-Liang Li, Ai-Bing Wang, Yue Huang, De-Pei Liu, Chiming Wei, G. Metville Williams, Chan-Na Zhang, Guang Liu, Yu-Qing Liu, De-Long Hao, Rui-Tai Hui, Mao Lin, Chih-Chuan Liang,