Shexiang baoxin pill protects against myocardial infarction induced chronic heart failure by activating energy metabolism via modulating mitochondrial biogenesis

Background The disease known as myocardial infarction (MI)-induced chronic heart failure (CHF) is actually brought on by an imbalance in the energy metabolism of the heart's supply and demand, which eventually leads to aberrant cardiac cell function and structure. An imbalance in energy metabolism is a major contributor to the pathological process of MI-induced CHF. Strengthening myocardial energy metabolism is a novel approach to treating CHF caused by MI. One well-known traditional Chinese medicine recipe, shexiang baoxin pill (SBP), offers good clinical therapeutic effects on cardiovascular disorders. Uncertainty exists regarding SBP's impact on CHF's energy metabolism following MI. In this work, we investigated the regulatory effects of SBP on energy metabolism in mice with CHF caused by MI using a variety of research strategies. Methods By ligating the left anterior descending coronary artery with silk thread, a mouse model of acute myocardial infarction (MI) was created. The success of the MI-induced HF model was verified by collecting the chocardiographic data. Afterwards, four distinct groups of mice were randomly assigned: HF, SBP, sham, and positive control (enalapril) groups. The technique utilized to assess heart function was echocardiography. Cardiac tissue necrosis and myocardial fibrosis were examined using H&E and Masson taining. Myocardial ATP levels were measured using colorimetry. The levels of NT-proBNP, MDA, and SOD were estimated by ELISA. Lastly, the expression levels of PGCα, NRF1, and TFAM in the myocardium were investigated using Western blotting and real-time fluorescence quantitative PCR (RT-qPCR). Results Treatment with SBP decreased oxidative stress and myocardial cell damage brought on by MI-induced CHF, while also improving remodeling of ventricular and cardiac function. Furthermore, ATP synthesis was reduced in MI-induced CHF along with alterations in the expression of genes associated to mitochondrial biosynthesis and mitochondrial respiratory function; all of these effects were considerably mitigated by SBP therapy. Conclusion Through energy metabolism modulation, SBP restores the cardiac dysfunction and myocardial structural integrity caused by MI. It's possible that SBP's regulatory influence on energy metabolism is connected to its positive reinforcement of mitochondrial biosynthesis.