4.7 Article

Purple rice anthocyanin extract protects cardiac function in STZ-induced diabetes rat hearts by inhibiting cardiac hypertrophy and fibrosis

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 31, 期 -, 页码 98-105

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2015.12.020

关键词

Diabetes mellitus; Anthocyanin; Cardiomyopathy; Cardiac inflammation; Cardiac fibrosis

资金

  1. Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence [MOHW104-TDU-B-212-113002]

向作者/读者索取更多资源

Diabetes mellitus (DM) often causes chronic inflammation, hypertrophy, apoptosis and fibrosis in the heart and subsequently leads to myocardial remodeling, deteriorated cardiac function and heart failure. Anthocyanins are strong antioxidants that show effective cardioprotective properties. Our aim was to determine whether anthocyanin extracted from purple rice provides protective effects in DM hearts. Five-week-old male Wistar rats were administered with streptozotocin (STZ) to induce type 1 diabetes. Animals were randomly divided into normal group, DM group (induced by 55 mg/kg STZ, i.p.) and DM with anthocyanin group (250 mg/kg/day, feeding 4 weeks). After treatment, the left ventricular tissues were collected to observe the relevant changes in the heart and the associated molecular events were determined by Western blotting assay. STZ-induced DM increased the proinflammatory signaling proteins in the heart and triggered the development of cardiac hypertrophy and fibrosis. Significant reduction in the heart function index such as left ventricular end-diastolic dimension and left ventricular end-systolic dimension was observed in the STZ-induced DM rat hearts, suggesting myocardial tissue damage and loss of heart function. Treatment with anthocyanin from purple rice extract, however, reduced the effect of DM and showed significant reduction in cardiac hypertrophy and fibrosis. Anthocyanin therefore restores the deteriorating cardiac functions in DM rats as evident from their heart functional parameters. (C) 2016 Elsevier Inc. All rights reserved.

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