Traditional Chinese medicine for regulating HF mitochondrial function and energy metabolism

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Traditional Chinese medicine study on lipid metabolism showed that QSYQ treatment mitigated DOX-induced heart damage and prevented structural damage to the heart. DOX damages cardiac function by reducing the protein content of ATP 5D, PPARα, and peroxisome proliferator-activated receptor

Pumping blood to meet the body's needs depends heavily on the supply of adenosine triphosphate (ATP). The oxidation of nutrients including fatty acids, glucose, lactic acid, ketone bodies, and amino acids is the source of ATP. Fatty acids provide 70 to 90 percent of the heart's ATP. Glucose, lactic acid, and a small number of amino acids provide the remaining 10% to 30% of ATP required by the heart. [119] Because lipid metabolism dominates the heart's energy supply, much research has focused on regulating it to treat heart disease. Peroxisome proliferator-activated receptor α (PPARα) is involved in the whole process of lipid metabolism and has been widely studied. Activation of PPARα reduces plasma levels of very low density lipoprotein (VLDL), which inhibits the formation of triglycerides and cholesterol [120121]. Therefore, activation of PPARα by agonists is a potential strategy for the treatment of coronary heart disease. Traditional Chinese medicine has the function of regulating cardiometabolism and protecting heart in treating heart failure. Previous studies have shown that DQP significantly upregulates PPARα expression in AMI models [72]. Our study also shows that DQP can regulate the expression of apolipoprotein A-I (ApoA-I), differentiated cluster 36 (CD36), fatty acid-binding protein (FABP), carnitine palmitoyl transferase I (CPT-1A), and lipoprotein lipase (LPL) in cardiac tissue. In conclusion, DQP has a comprehensive regulatory effect on the lipid metabolism process in AMI rats.

Another traditional Chinese medicine study on lipid metabolism showed that QSYQ treatment mitigated DOX-induced heart damage and prevented structural damage to the heart. DOX damages cardiac function by reducing the protein content of ATP 5D, PPARα, and peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) [123]. Meanwhile, a parallel study found that after 7 days of QSYQ pretreatment, ATP levels and mitochondrial transmembrane potential (MTP) were restored in AMI hearts. QSYQ pretreatment can also regulate plasma SOD, MDA, TNF-α and IL-1α. QSYQ improves energy metabolism and reduces oxidative stress by alleviating I/ R-induced mitochondrial abnormalities [124]. The effect of QSYQ on energy metabolism was studied by proteomics. The results showed that QSYQ treatment regulated the expression of proteins involved in oxidative stress and energy metabolism. Due to the interaction of its bioactive components, QSYQ has a better anti-hypertrophy effect than its single component or a combination of components. Of these components of QSYQ, 3, 4-dihydroxy-phenyllactic acid is the best candidate to combat oxidative stress. Astragaloside IV and notoginseng saponin R1 are more effective in regulating energy metabolism [125]. Another well-known prescription, Shenfu Decoction, was found to have therapeutic effects on chronic HF rats. Urine and plasma metabolomics results showed that inflammation and energy metabolism dysfunction were associated with 16 potential urine biomarkers and 13 potential plasma biomarkers. Accessory decoration can partially restore the disturbed pathway of differentially expressed biomarker enrichment.

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