Shengmai Yin active ingredients bind tightly to diesel exhaust particulate matter components (binding energies < -5 kcal/mol), targeting the lipid and atherosclerosis pathway.
Network pharmacology and molecular docking suggest Shengmai Yin may treat diesel exhaust-induced myocardial hypertrophy by targeting the lipid and atherosclerosis pathway.
Background: Previous studies have shown that diesel exhaust particulate matter (DPM) can cause lung damage, which in turn leads to myocardial hypertrophy. However, the mechanism of cross-organ damage remains unclear. The traditional Chinese medicine compound Shengmai Yin (SMY) has excellent therapeutic effects on both heart and lung diseases. In this study, using network toxicology/pharmacology and molecular docking techniques, we explored the potential mechanism of SMY in treating cross-organ damage induced by DPM. Methods: We retrieved the target genes related to lung injury and hypertrophic cardiomyopathy from comparative toxicogenomics database and GeneCards and used TCMSP and SymMap databases to obtain the compounds related to SMY and their targets. Cross-analysis using Venn diagrams, STRING, and Cytoscape revealed potential targets and key pathways for myocardial hypertrophy induced by DPM and the therapeutic effects of SMY. Results: Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that both heart and lung injuries induced by DPM are associated with lipid metabolism regulation. The core pathway for SMY treatment targets was also shown to be the “Lipid and Atherosclerosis Pathway,” and it was discovered that active components in SMY, such as Ginsenoside Rh2, Diosgenin, beta-sitosterol, Gomisin-A, and Stigmasterol, have regulatory effects on this pathway. Hub targets such as tumor necrosis factor, tumor protein p53, peroxisome proliferator-activated receptor gamma, BCL2 apoptosis regulator, and toll-like receptor 4 were also identified. Molecular docking results showed that key components of DPM could bind tightly with the active ingredients of the SMY, with binding energies all less than −5 kcal/mol, indicating high binding capacity. Conclusion: This study provides a theoretical basis for revealing the role of SMY in treating DPM-induced myocardial hypertrophy and promotes the application of network toxicology and molecular docking technology in environmental pollutant research.
Qu et al. (Thu,) conducted a other in Diesel exhaust particulate matter-induced myocardial hypertrophy. Shengmai Yin (SMY) was evaluated on Molecular docking binding energies. Shengmai Yin active ingredients bind tightly to diesel exhaust particulate matter components (binding energies < -5 kcal/mol), targeting the lipid and atherosclerosis pathway.