ginsenoside-rg2 has been researched along with Fibrosis* in 2 studies
2 other study(ies) available for ginsenoside-rg2 and Fibrosis
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Ginsenoside Rg2 alleviates myocardial fibrosis by regulating TGF-β1/Smad signalling pathway.
This study investigates the effect of ginsenoside Rg2 on myocardial fibrosis in myocardial ischaemia rats.. Compared with myocardial ischaemic rats, ginsenoside Rg2 at doses of 5, 20 mg/kg abated partially the augment of LVEDP (8.9 ± 1.3 vs. 7.5 ± 0.7, 7.2 ± 1.0 mmHg) and the decreases of the LVSP (96.75 ± 13.2 vs. 118.3 ± 19.4, 124.3 ± 21.3 mmHg), the + dp/dt (2142.8 ± 309.3 vs. 2598.6 ± 404.0, 2661.5 ± 445.2 mmHg/s), and the -dp/dt (1996.3 ± 306.3 vs. 2476.6 ± 289.7, 2509.6 ± 353.1 mmHg/s). Ginsenoside Rg2 (9.2 ± 0.9%, 8.5 ± 0.8%) alleviated myocardial fibrosis when compared with the isoproterenol group (10.1 ± 1.0%), which was accompanied by suppressed TGF-β1/Smad signalling in heart tissues.. Ginsenosides from ginseng possess the property of alleviating myocardial fibrosis, improving cardiac function after myocardial ischaemia. Ginsenosides may be promising agents for improving the outcomes of patients with myocardial ischaemia. Topics: Animals; Cardiotonic Agents; Dose-Response Relationship, Drug; Fibrosis; Ginsenosides; Isoproterenol; Male; Myocardial Ischemia; Panax; Rats; Rats, Wistar; Signal Transduction; Smad Proteins; Transforming Growth Factor beta1 | 2021 |
Ginsenoside Rg2 attenuates myocardial fibrosis and improves cardiac function after myocardial infarction via AKT signaling pathway.
With the popularization of percutaneous coronary intervention technology in clinical applications, the mortality rate of acute myocardial infarction has been significantly reduced. However, ventricular remodeling following myocardial infarction (MI) has attracted extensive attention for that it can cause malignant arrhythmia, heart failure, and even death. We aimed to investigate the effects of ginsenoside Rg2 on cardiac function and myocardial fibrosis after MI and its potential mechanism. The results demonstrated that ginsenoside Rg2 improved cardiac function and inhibited collagen deposition in mice after MI. In addition, ginsenoside Rg2 reduced the levels of fibrosis-associated genes Collagen I (Col 1), Collagen III (Col 3), and alpha-smooth muscle actin (α-SMA) by activating phosphorylated AKT in angiotensin II-induced cardiac fibroblasts. Taken together, ginsenoside Rg2 improves cardiac function and attenuates cardiac fibrosis via the AKT pathway, suggesting that ginsenoside Rg2 may be a promising drug for the prevention of ventricular remodeling after MI. Topics: Animals; Collagen Type I; Fibrosis; Ginsenosides; Heart; Myocardial Infarction; Myocardium; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Signal Transduction; Ventricular Remodeling | 2020 |