Abstract Title:

Protective effects of tannic acid on pressure overload-induced cardiac hypertrophy and underlying mechanisms in rats.

Abstract Source:

J Pharm Pharmacol. 2017 Sep ;69(9):1191-1207. Epub 2017 Jun 20. PMID: 28631819

Abstract Author(s):

Li Chu, Pinya Li, Tao Song, Xue Han, Xuan Zhang, Qiongtao Song, Tao Liu, Yuanyuan Zhang, Jianping Zhang

Article Affiliation:

Li Chu


OBJECTIVES: The aim of this study was to examine the cardioprotective effects and latent mechanism of tannic acid (TA) on cardiac hypertrophy.

METHODS: Abdominal 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 FINDINGS: Abdominal 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 (AT1 R), angiotensin type 2 receptor (AT2 R), phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and transforming growth factor-β (TGF-β) 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-α (TNF-α), interleukin-1β (IL-1β), bax, caspase-3 and upregulated expression of bcl-2.

CONCLUSIONS: Tannic 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.

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