Heart muscle cell enlargement, referred to as myocardial hypertrophy, serves as a critical disease process observed in the cardiomyopathy phase that appears after patients undergo anthracycline medication. The capacity of ginsenoside Rb1 (Rb1) to influence hypertrophy caused by these agents has not been determined clearly until now. The goal of the present research was to test the ability of Rb1 to counteract heart muscle cell growth in the period following doxorubicin (DOX) exposure while also clarifying the biological route through which it might act. The model of myocardial hypertrophy in the post-DOX phase was produced by giving C57BL/6 mice a 15 mg/kg injection of DOX and then studying the hearts after 12 days or after 22 hours. Parallel cell experiments used H9c2 cardiomyoblasts incubated with 2 μM DOX for a 2-hour period. Rb1 was supplied to the mice beginning two days ahead of DOX and continued once daily across a 14-day span. In the cell work, Rb1 exposure started 6 hours in advance of DOX and lasted through a total 30-hour incubation. Hypertrophy indicators tracked included heart weight relative to body weight (HW/BW), heart weight relative to tibia length (HW/TL), ultrasound heart imaging, WGA-based cell size staining, plus measurement of α-SMA, BNP, and β-MHC protein amounts. Heart tissue shape and structure were inspected using HE staining, Masson staining, and electron microscope imaging. Free calcium inside cells was quantified through Fluo-3/AM dye fluorescence. Levels and location of proteins in the CaNBβ/NFATc4/GATA4 route were studied with Western blot analysis, tissue staining by immunohistochemistry, and cell staining by immunofluorescence. Rb1 application caused notable lowering of the HW/BW ratio, HW/TL ratio, and LVd mass/BW ratio. It also shrank the average size of heart muscle cells and brought down the production of BNP, β-MHC, and α-SMA. Rb1 further decreased the amount of scar-like fibrous tissue in the heart, helped restore normal tiny structures inside cells, and supported improved blood flow dynamics in the hearts of DOX-exposed mice. Calcium excess that normally follows DOX was also reduced by Rb1. Matching these protective changes, the unusually high amounts of CaN, NFATc4, and GATA4 proteins detected in both animal and cell experiments returned toward normal. Rb1 lessened the myocardial hypertrophy that occurs after doxorubicin is given. This improvement is likely related to reduced functioning of the CaN/NFAT/GATA4 molecular pathway.
