Potential Cardioprotective Mechanisms of Bawu Junzi Decoction in Myocardial Infarction: Identification of CYP1B1 and ALDH2 as Key Mediators

Background Bawu Junzi (BWJZ) decoction, shows efficacy in treating myocardial infarction (MI) but the specific mechanism remains unclear. This study aims to identify the therapeutic targets and mechanisms of BWJZ decoction against MI. Methods After preparing BWJZ decoction, the supernatant was collected for LC-MS/MS detection. Active substances were identified by screening chemical components from the TCMSP database. Targets of active components were predicted using the SwissTargetPrediction database. Differentially expressed genes (DEGs) between the MI and control groups were calculated using the limma package, and key genes were identified by intersecting these DEGs with mitochondria energy metabolism-related genes (MMRGs) and predicted targets of the active substances. Key genes were further validated using in vitro experiments. Enrichment analysis was performed using the clusterProfiler package. Molecular docking was performed using AutoDock Vina software. However, this study lack in vivo animal validation, clinical evidence or in-depth molecular mechanism elucidation. Results Differential analysis identified 409 DEGs, among which aldehyde dehydrogenase 2 ( ALDH2) and cytochrome P450 family 1 subfamily B member 1 ( CYP1B1) were the intersection genes used to develop a PPI network. In vitro , ALDH2 overexpression promoted cell viability, ATP, and SOD while reducing apoptosis, MDA, IL-6, and TNF-α. Similarly, CYP1B1 silencing increased cell viability and ATP. High-expression groups of ALDH2 and CYP1B1 were significantly enriched in immune-related pathways. Molecular docking revealed that both liquiritigenin and hesperetin bound stably within the active pocket of CYP1B1 . Conclusion This study provides a novel strategy for natural product-based interventions targeting immune-related pathways.