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

心室 射血分数 心肌纤维化 纤维化 医学 肿瘤坏死因子α NF-κB 内科学 化学 内分泌学 心力衰竭 炎症 信号转导 生物化学
作者
Shiye Ke,Dinghui Liu,Lin Wu,Xianguan Yu,Sheng Wang,Guangyao Shi,Ren-Hui Wen,Bin Zhou,Baoshun Hao,Yong Liu,Jieming Zhu,Xiaoxian Qian
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:48 (06): 1369-1383 被引量:8
标识
DOI:10.1142/s0192415x20500676
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-[Formula: see text]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-[Formula: see text]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-[Formula: see text] levels. Furthermore, Rb1 treatment in aged mice increased cytoplasmic NF-[Formula: see text]B but decreased nuclear NF-[Formula: see text]B, which indicated the suppression of the NF-[Formula: see text]B signaling pathway by regulating the translocation of NF-[Formula: see text]B. Rb1 could alleviate aging-related myocardial dysfunction by suppressing fibrosis and inflammation, which is potentially associated with regulation of the NF-[Formula: see text]B signaling pathway.
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