Author + information
- Si-Chi Xu and
- Qi-Zhu Tang
Cardiac remolding is characterized as left ventricular dilatation, cardiac fibrosis, and impaired systolic function which predisposes the affected individuals to heart failure. Previous studies had demonstrated thatperoxisome proliferator activated receptor α played key roles in the development of cardiovascular disease by modulate cardiac energy metabolism. Whether BZA could protect pressure overload-induced remodeling has not been completely identified yet.
The mice were orally given Bezafibrate (BZA) (100mg/kg) from 1 week to 8 weeks after aortic banding (AB). Cardiac function was assessed by echocardiographic parameters including left ventricular diastolic diameter (LVDD), left ventricular ejection fraction (LVEF), and fractional shortening (FS). Body weight (BW), heart weight (HW), and tibia length (TL) were also examined. HE and PSR staining were used to evaluate cross sectional area (CSA) and fibrosis. The hypertrophic and collagen markers were quantitatively determined by RT-PCR. Western blot was applied to detect the expressions of proteins.
BZA could decrease LVDD and increase LVEF and FS compared with sham group. Pressure overload resulted in increased HW/BW and HW/TL, while BZA restricted the elevated HW/BW and HW/TL. Decreased CSA and hypertrophic markers were also observed in mice subjected to AB+BZA. BZA also attenuated AB-induced cardiac fibrosis, as illustrated by the decreased collagen volume and fibrotic markers. We also found that the phosphorylation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinase (MAPK) were significantly downregulated under the BZA treatment.
Our study demonstrated that BZA could alleviate cardiomyocyte hypertrophy and suppress cardiac fibrosis in mice.