Bawei Chenxiang Wan (BCW), a well-known traditional Chinese
Tibetan medicine formula, is effective for the treatment of acute and chronic
cardiovascular diseases. In the present study, we investigated the effect of BCW in
cardiac hypertrophy and underlying mechanisms. The dose of 0.2, 0.4, and 0.8 g/kg BCW treated
cardiac hypertrophy in SD rat model induced by
isoprenaline (ISO). Our results showed that BCW (0.4 g/kg) could repress
cardiac hypertrophy, indicated by macro morphology, heart weight to
body weight ratio (HW/BW), left ventricle heart weight to
body weight ratio (LVW/BW),
hypertrophy markers, heart function, pathological structure, cross-sectional area (CSA) of myocardial cells, and the myocardial
enzymes. Furthermore, we declared the mechanism of BCW anti-
hypertrophy effect was associated with activating
adenosine 5'-monophosphate (
AMP)-activated protein kinase (AMPK)/
peroxisome proliferator-activated receptor-α (
PPAR-α) signals, which regulate
carnitine palmitoyltransferase1β (CPT-1β) and
glucose transport-4 (GLUT-4) to ameliorate
glycolipid metabolism. Moreover, BCW also elevated
mitochondrial DNA-encoded genes of
NADH dehydrogenase subunit 1(ND1),
cytochrome b (Cytb), and mitochondrially encoded
cytochrome coxidase I (mt-co1) expression, which was associated with mitochondria function and oxidative phosphorylation. Subsequently, knocking down AMPK by
siRNA significantly can reverse the anti-
hypertrophy effect of BCW indicated by
hypertrophy markers and cell surface of cardiomyocytes. In conclusion, BCW prevents ISO-induced cardiomyocyte
hypertrophy by activating AMPK/
PPAR-α to alleviate the disturbance in energy metabolism. Therefore, BCW can be used as an alternative drug for the treatment of
cardiac hypertrophy.