Ginsenoside Rb1 Ameliorates Age-Related Myocardial Dysfunction by Regulating the NF-κB Signaling Pathway

被引:10
作者
Ke, Shi-Ye [1 ,3 ]
Liu, Ding-Hui [1 ,2 ]
Wu, Lin [1 ]
Yu, Xian-Guan [1 ]
Wang, Min [1 ]
Shi, Guang-Yao [1 ]
Wen, Ren-Hui [1 ]
Zhou, Bin [1 ]
Hao, Bao-Shun [1 ]
Liu, Yong [1 ]
Zhu, Jie-Ming [1 ]
Qian, Xiao-Xian [1 ,2 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Cardiol, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Inst Integrated Tradit Chinese & Western Med, Guangzhou 510630, Guangdong, Peoples R China
[3] Sun Yat Sen Univ, Affiliated Hosp 8, Dept Cardiol, Shenzhen 518000, Guangdong, Peoples R China
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2020年 / 48卷 / 06期
基金
中国国家自然科学基金;
关键词
Ginsenoside Rb1; Aged Mice; Cardiac Fibrosis; Inflammation; NF-kappa B Signaling Pathway; OXIDATIVE STRESS; CARDIAC DYSFUNCTION; HEART; INFLAMMATION; APOPTOSIS; CARDIOMYOPATHY; MITOCHONDRIAL; EXPRESSION; MEDIATORS; ARTERIAL;
D O I
10.1142/S0192415X20500676
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Age-related myocardial dysfunction is a very large healthcare burden. Here, we aimed to investigate whether ginsenoside Rb1 (Rb1) improves age-related myocardial dysfunction and to identify the relevant molecular mechanism. Young mice and aged mice were injected with Rb1 or vehicle for 3 months. Then, their cardiac function was inspected by transthoracic echocardiography. Serum and myocardium tissue were collected from all mice for histological or molecular expression analyses, including aging-related proteins, markers relevant to fibrosis and inflammation, and markers indicating the activation of the nuclear factor-kappa B (NF-kappa B) pathway. Compared with the control condition, Rb1 treatment significantly increased the ejection fraction percentage and significantly decreased the internal diameter and volume of the left ventricle at the end-systolic and end-diastolic phases in aged mice. Rb1 treatment reduced collagen deposition and collagen I, collagen III, and transforming growth factor-beta 1 protein expression levels in aged hearts. Rb1 also decreased the aging-induced myocardial inflammatory response, as measured by serum or myocardial interleukin-6 and tumor necrosis factor-alpha levels. Furthermore, Rb1 treatment in aged mice increased cytoplasmic NF-kappa B but decreased nuclear NF-kappa B, which indicated the suppression of the NF-kappa B signaling pathway by regulating the translocation of NF-kappa B. Rb1 could alleviate aging-related myocardial dysfunction by suppressing fibrosis and inflammation, which is potentially associated with regulation of the NF-kappa B signaling pathway.
引用
收藏
页码:1369 / 1383
页数:15
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