Effects of Ginsenoside on Atrial Fibrillation in Rats with Heart Failure after Myocardial Infarction

被引：0
作者：
Chen Xiaoli [1 ]
Liu Xiaoli [2 ]
Luo Zhi [1 ]
Zhang Yi [3 ]
Bai Ying [1 ]
Jia Ding [1 ]
Feng Shixing [1 ]
机构：
[1] Beijing Geriatr Hosp, Dept Cardiol, Beijing 100095, Peoples R China
[2] Capital Med Univ, Dept Cardiol, Beijing Anzhen Hosp, Beijing 100029, Peoples R China
[3] Beijing Geriatr Hosp, Dept Sci & Educ, Beijing 100095, Peoples R China
来源：
LATIN AMERICAN JOURNAL OF PHARMACY | 2018年 / 37卷 / 12期
关键词：
atrial fibrillation; atrial fibrosis; ginsenoside; Nrf2; EXPRESSION; THERAPY; LIVER;
D O I：
暂无
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
The object was to investigate the effects and mechanisms of ginsenoside on atrial fibrillation (AF) in rats with heart failure (HF) after myocardial infarction (MI). 24 HF rats were randomly divided into HF group (CF) and Treatment group which were treated with ginsenoside (Treatment) (n = 12, respectively). Ten sham operation control rats were grouped into sham group (Sham). The Treatment group was treated with ginsenoside (10 mg/kg), and the other groups were administrated with the normal saline. After four weeks intervention, echocardiography, AF vulnerability, atrial fibrosis, connexin 43, PI3K, AKT, Nrf2 protein expression were assessed. Ginsenoside resulted in an attenuation of arrhythmogenic left atrial remodeling, with a significant reduction in left atrial diameter (P < 0.01), AF inducibility and duration, and atrial fibrosis (P < 0.05), and an increase of protein expression of Cx43 and up-regulation of PI3k/Akt/Nrf2 signaling pathway (P < 0.05). Ginsenoside has the potential to reduce arrhythmogenic atrial remodeling and AF vulnerability via anit-fibrosis, inhibiting gap junction remodeling by up-regulating PI3K/AKT/Nrf2 signaling pathway.
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页码：2388 / 2394
页数：7
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