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Vinpocetine Attenuates Pathological Cardiac Remodeling by Inhibiting Cardiac Hypertrophy and Fibrosis 期刊论文

编号：

56929aa1-c666-4903-9274-237ec0f286e3
作者：

Wu, Meiping(吴美平)#^[1,2]Zhang, Yishuai#^[2]Xu, Xiangbin^[3];Zhou, Qian^[2];Li, JianDong*^[4]Yan, Chen*^[1,2]
语种：

英文
期刊：

CARDIOVASCULAR DRUGS AND THERAPY ISSN：0920-3206 2017 年 31 卷 2 期 (157 - 166) ; APR
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关键词：

Vinpocetine Cardiac remodeling Cardiac hypertrophy Cardiac fibrosis PDE1
摘要：

Pathological cardiac remodeling, characterized by cardiac hypertrophy and fibrosis, is a pathological feature of many cardiac disorders that leads to heart failure and cardiac arrest. Vinpocetine, a derivative of the alkaloid vincamine, has been used for enhancing cerebral blood flow to treat cognitive impairment. However, its role in pathological cardiac remodeling remains unknown. The aim of this study is to examine the effect of vinpocetine on pathological cardiac remodeling induced by chronic stimulation with angiotensin II (Ang II).
Mice received Ang II infusion via osmotic pumps in the presence of vehicle or vinpocetine. Cardiac hypertrophy and fibrosis were assessed by morphological, histological, and biochemical analyses. Mechanistic studies were carried out in vitro with isolated mouse adult cardiac myocytes and fibroblasts.
We showed that chronic Ang II infusion caused cardiac hypertrophy and fibrosis, which were all significantly attenuated by systemic administration of vinpocetine. In isolated adult mouse cardiomyocytes, vinpocetine suppressed Ang II-stimulated myocyte hypertrophic growth. In cultured cardiac fibroblasts, vinpocetine suppressed TGF beta-induced fibroblast activation and matrix gene expression, consistent with its effect in attenuating cardiac fibrosis. The effects of vinpocetine on cardiac myocyte hypertrophy and fibroblast activation are likely mediated by targeting cyclic nucleotide phosphodiesterase 1 (PDE1).
Our results reveal a novel protective effect of vinpocetine in attenuating pathological cardiac remodeling through suppressing cardiac myocyte hypertrophic growth and fibroblast activation and fibrotic gene expression. These studies may also shed light on developing novel therapeutic agents for antagonizing pathological cardiac remodeling.
推荐引用方式
GB/T 7714：

Wu Mei-ping,Zhang Yi-shuai,Xu Xiangbin, et al. Vinpocetine Attenuates Pathological Cardiac Remodeling by Inhibiting Cardiac Hypertrophy and Fibrosis [J].CARDIOVASCULAR DRUGS AND THERAPY,2017,31(2):157-166.
APA：

Wu Mei-ping,Zhang Yi-shuai,Xu Xiangbin,Zhou Qian,&Yan Chen.(2017).Vinpocetine Attenuates Pathological Cardiac Remodeling by Inhibiting Cardiac Hypertrophy and Fibrosis .CARDIOVASCULAR DRUGS AND THERAPY,31(2):157-166.
MLA：

Wu Mei-ping, et al. "Vinpocetine Attenuates Pathological Cardiac Remodeling by Inhibiting Cardiac Hypertrophy and Fibrosis" .CARDIOVASCULAR DRUGS AND THERAPY 31,2(2017):157-166.
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