کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8268377 | 1534954 | 2015 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protective effect of cilostazol against doxorubicin-induced cardiomyopathy in mice
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کلمات کلیدی
AMPKTLR4LVEDdHMGB1LVESDBNPSOD-1PDECTGFHO-1DICDOXAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده استhigh-mobility group box 1 - جعبه گروه تحریر بالا 1Doxorubicin - دوکسوروبیسینFree radicals - رادیکال آزادSuperoxide dismutase-1 - سوپراکسید دیسموتاز-1Cilostazol - سیلوستازولConnective tissue growth factor - فاکتور رشد بافت همبندPhosphodiesterase - فسفو دی استرازMouse - موشheme oxygenase 1 - همای اکسیژناز 1B-type natriuretic peptide - پپتید نیترویوتیک B نوعCardiomyopathy - کاردیومیوپاتیToll-like receptor 4 - گیرنده تله مانند 4
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Protective effect of cilostazol against doxorubicin-induced cardiomyopathy in mice Protective effect of cilostazol against doxorubicin-induced cardiomyopathy in mice](/preview/png/8268377.png)
چکیده انگلیسی
Doxorubicin (Dox) is an effective anti-cancer drug, but its use is limited because of its adverse effect of inducing irreversible dilated cardiomyopathy. Cilostazol (Cilo), a potent phosphodiesterase III inhibitor, has been reported to have an anti-inflammatory effect. Here, we investigated whether Cilo has a protective effect against Dox-induced cardiomyopathy (DIC). Mice were randomly divided into four groups: saline control, Dox (15 mg/kg), Dox (15 mg/kg) plus Cilo (50 mg/kg), and Cilo (50 mg/kg). The results showed that the coadministration of Dox and Cilo significantly enhanced left-ventricular systolic function compared with Dox alone. In addition, Cilo treatment significantly reduced Dox-induced perivascular fibrosis, collagen concentration, and connective growth factor expression in the heart. Also, Cilo administration markedly reduced Dox-induced levels of serum B-type natriuretic peptide, dysferlin, high-mobility group protein B1, Toll-like receptor 4, nuclear factor-κB p65, and cyclooxygenase-2. Furthermore, Cilo treatment significantly reduced Dox-induced oxidative stress by lowering the translocation of Nrf2 into the nucleus and the expression of NQO1, heme oxygenase 1, and superoxide dismutase-1. Our results suggest that Cilo may be a potential antifibrotic, antioxidative, and anti-inflammatory drug for DIC.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 89, December 2015, Pages 54-61
Journal: Free Radical Biology and Medicine - Volume 89, December 2015, Pages 54-61
نویسندگان
Jin Sin Koh, Chin-ok Yi, Rok Won Heo, Jong-Wha Ahn, Jeong Rang Park, Jung Eun Lee, Jung-Hwan Kim, Jin-Yong Hwang, Gu Seob Roh,