DOI: https://doi.org/10.2478/acph-2026-0006
Article ID: 260006 (12 pages)
Acta Pharm. 76(1) (2026)
Short communication
The effect of astragaloside IV on a model of isoproterenol-induced hypertrophic injury in H9c2 cells
YANG LONG, YUAN XIAO, CHUN CHEN, CHAO PENG, YUXI ZHANG
Abstract
The objective of this study was to explore the protective effect of astragaloside IV on a model of isoproterenol-induced (ISO) hypertrophic injury in rat cardiomyocytes H9c2 (cell line derived from embryonic BD1X rat heart tissue). A cell hypertrophy injury model was established (H9c2 cells treated with 100 μmol L–1 ISO). The cells were divided into normal control, a model group, and an astragaloside IV group at several concentrations. Astragaloside IV was pre-administered for 2 hours, followed by ISO treatment for 24 hours. Cell viability, cell surface area, apoptosis rate, lactate dehydrogenase (LDH) activity, reactive oxygen species (ROS), superoxide dismutase (SOD), the mRNA levels of Bcl-2, Bax, p62, and LC3, the protein expressions of Sirt1, p62, caspase-3, beclin, and p53 and the LC3Ⅱ/LC3Ⅰ ratio were detected. Astragaloside IV significantly alleviated ISO-induced hypertrophy injury in H9c2 cells, reduced cell surface area and LDH release, decreased apoptosis rate and intracellular ROS levels, increased SOD levels, upregulated the expressions of autophagy-related mRNA and proteins, and downregulated the expressions of apoptosis-related mRNA and proteins. Astragaloside IV can effectively inhibit ISO-induced hypertrophy and apoptosis in H9c2 cells, and its mechanism may be related to promoting autophagy and reducing oxidative stress.
Keywords
astragaloside IV, cardiac hypertrophy, apoptosis, autophagy, oxidative stress
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