Aconiti Lateralis Radix Praeparata (
Fuzi), a type of Chinese
materia medica, has been used to treat acute and chronic
heart failure (HF) in
traditional Chinese medicine and has been proven in numerous animal studies. It is also well-known that
Zingiberis Rhizoma (
Ganjiang) is ineffective in the treatment of HF, but it can enhance the anti-HF effect of
Fuzi. However, the mechanism underlying this compatibility is still not well investigated. To investigate this mechanism, a model of acute
heart failure (AHF) in SD rats induced by
propafenone hydrochloride was established in this study. After oral treatments of
Ganjiang,
Fuzi or a combination of the two drugs in rats with AHF, heart function [e.g., heart rate (HR) and the maximal rising and declining rate of left ventricle pressure (±dp/dtmax)] and serum indicators [e.g.,
brain natriuretic peptide (BNP),
lactate dehydrogenase (LDH) and
creatine kinase (CK)] were measured, and histopathological analysis of the heart was also performed. The biological mechanisms were further explored by measuring the
protein expression level of the mitochondrial respiration chain complex (MRCC1-4) and the
mRNA and
protein expression levels of mitochondrial Ca2+ uniporter (MCU) and its upstream
proteins, mitochondrial Ca2+ uniporter 1 and mitochondrial Ca2+ uniporter 2 (MICU1-2). The expression levels of key
enzymes downstream of the tricarboxylic acid cycle, including
pyruvate dehydrogenase (PDH),
malate dehydrogenase (MDH) and
nicotinamide nucleotide transhydrogenase (NNT), were also measured. As a result,
Ganjiang enhanced the
therapeutic effect of
Fuzi on AHF by raising the HR and ±dp/dtmax; decreasing the serum levels of BNP, LDH and CK; and alleviating histological damage of the myocardial tissue when compared to the treatments of
Ganjiang or
Fuzi alone. In conclusion, there was an enhancing effect of
Ganjiang on the anti-AHF function of
Fuzi treatment, and the potential mechanism of this effect may be related to the mitochondrial energy metabolism pathway mediated by MCU.