Panax ginseng exerts cardioprotective effect post myocardial infarction by attenuating myocardial fibrosis and inflammation through SIRT1 signaling pathways

作者：Honglin Xu, Mingjie Pang, Changlei Hu, Tong Xu, Guang‐Hong Chen, Guoyong Zhang, Xin Han, Yue Hua, Yuting Wu, Jiayi Zhang, Yiming Bi, Bin Liu, Yingchun Zhou · 发表于：Journal of Ginseng Research · 年份：2025 · DOI：10.1016/j.jgr.2025.01.001 · 被引用次数：15 · 研究领域：Ginseng Biological Effects and Applications、Inflammasome and immune disorders、Medicinal Plants and Bioactive Compounds

Myocardial fibrosis and inflammation induce adverse cardiac remodeling post-myocardial infarction (MI). Panax ginseng ( P. ginseng ) is beneficial for diverse cardiovascular diseases. However, the therapeutic effect and molecular mechanism underlying cardiac remodeling are largely unclear. A MI mouse model was constructed through permanent left anterior descending (LAD) coronary artery ligation. TGF-β1 or LPS was used for stimulating cardiac fibroblasts (CFs) or RAW264.7 macrophages to construct the collagen synthesis and inflammation model in vitro . The cardiac structure and function were detected through hematoxylin-eosin staining, Masson staining, and echocardiography, while myocardial fibrosis and inflammation markers were determined by Western-blot, immunohistochemistry, RT-PCR, and ELISA. Additionally, the Silent information regulator 1 (SIRT1)/nuclear factor-κB (NF-κB) mediated NOD like receptor 3 (NLRP3) inflammasome and TGFBR1/Smads signaling pathways were also evaluated. A SIRT1 selective inhibitor (EX-527) was used for confirming the pharmacological mechanism of P. ginseng . In vivo , P. ginseng alleviated ventricular remodeling, enhanced heart function, and ameliorated collagen I, collagen III, IL-1β, and IL-18 levels dose-dependently. Moreover, P. ginseng significantly suppressed NLRP3-caspase1 inflammasome and TGFBR1/Smads signaling in MI mice. In vitro , P. ginseng significantly suppressed collagen and inflammation markers, NLRP3 inflammasome and TGFBR1/Smads ...