Cardiac
fibrosis plays a causal role in the development of
heart failure, and anti-fibrotic
therapy represents a promising strategy to mitigate
heart failure. The purpose of this study was to investigate the effect of a new
drug-
liguzinediol on cardiac
fibrosis of
heart failure Male Sprague-Dawley rats (SD) rats and the underlying mechanisms.
Liguzinediol was administered to rats that were injected with
doxorubicin (Dox) for four weeks. Two weeks later, its effects on cardiac
fibrosis were assessed by haematoxylin and
eosin (HE) staining and Masson staining. The
collagen content was determined by Elisa, and
protein expression was detected by western blot in vitro and in vivo.
Liguzinediol decreased cardiac muscle fiber break evidenced by HE staining and it significantly reduced cardiac
fibrosis evidenced by Masson staining in DOX-treated rats. In addition, the
hydroxyproline level and the ratio of type I/III
collagens were also significantly decreased, and western blot assays showed that
liguzinediol regulated the balance between matrix matalloproteinases (
MMPs) and
tissue inhibitor of metalloproteinase (TIMPs) to protect cardiac remodeling in vivo and in vitro. These data collectively indicated that
liguzinediol could protect against cardiac
fibrosis in rats.
Liguzinediol could be exploited to be a promising candidate for cardiac
fibrosis.