期刊
JOURNAL OF PHARMACY AND PHARMACOLOGY
卷 69, 期 9, 页码 1191-1207出版社
WILEY
DOI: 10.1111/jphp.12763
关键词
cardiac hypertrophy; endothelin; oxidative stress; pressure overload; tannic acid
资金
- Nature Fund of Hebei Province, China [C2011206025]
- Fund of Hebei Science and Technology Bureau [10276105D-2]
ObjectivesThe aim of this study was to examine the cardioprotective effects and latent mechanism of tannic acid (TA) on cardiac hypertrophy. MethodsAbdominal aortic banding (AAB) was used to induce pressure overload-induced cardiac hypertrophy in male Wistar rats, sham-operated rats served as controls. AAB rats were treated with TA (20 and 40 mg/kg) or captoril. Key findingsAbdominal aortic banding rats that received TA showed ameliorated pathological changes in cardiac morphology and coefficients, decreased cardiac hypertrophy and apoptosis, a reduction in over expressions of angiotensin type 1 receptor (AT(1)R), angiotensin type 2 receptor (AT(2)R), phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and transforming growth factor- (TGF-) mRNA, and modified expression of matrix metal proteinase-9 (MMP-9) mRNA in AAB rat hearts. Furthermore, TA treatment contributed to a decrease in malondialdehyde (MDA) and endothelin-1 (ET-1) activities and content, while it caused an increase in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), nitric oxide (NO) and endothelial NO synthase (e-NOS). Furthermore, TA downregulated expression of tumour necrosis factor- (TNF-), interleukin-1 (IL-1), bax, caspase-3 and upregulated expression of bcl-2. ConclusionsTannic acid displayed obvious suppression of AAB-induced cardiac hypertrophy in rats. The cardioprotective effects of TA may be attributed to multitargeted inhibition of oxidative stress, inflammation, fibrosis and apoptosis in addition to an increase in NO levels, decrease in ET-1 levels, and downregulation of angiotensin receptors and the phosphorylation of ERK1/2.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据