Background: Astragaloside, which is one of the main components of
Astragalus membranaceus
, has been widely used
in the treatment of congestive heart failure in China, and it can protect cardiomyocytes. Its mechanism of action remains
unclear. Therefore, the present study was carried out to investigate the influence of
astragaloside on rat cardiomyocytes
stimulated with endothelin-1 (ET-1), and explored the underlying mechanism.
Materials and Methods: ET-1 was used to stimulate primary rat cardiomyocytes and establish a cardiomyocyte
hypertrophy model. Different
astragaloside doses were administered in combination with ET-1. Cardiomyocyte
hypertrophy and apoptosis were examined using transmission electron microscopy (TEM) and flow cytometry,
respectively. The molecular mechanism was explored by analyzing the mRNA of the vitamin D receptor (VDR),
cytochrome P450 family 27 subfamily B member 1(CYP27B), cytochrome P450 family 24 subfamily A member
1(CYP24A) and renin mRNA levels by quantificational real-time polymerase chain reaction(qRT-PCR).
Results: Rat cardiomyocyte hypertrophy model was established successfully.
Astragaloside administration significantly
affected cell apoptosis and significantly inhibited ET-1-induced cardiomyocyte hypertrophy in a dose-dependent manner.
Astragaloside treatment affected the expression of signaling molecules in the vitamin D axis.
Conclusion: Astragaloside inhibits ET-1-induced cardiomyocyte hypertrophy. This effect can be reversed by regulating
the levels of the relevant factors in the vitamin D axis.
