A Transcriptomic and Metabolomic Investigation of the Molecular Mechanism Underlying the Prevention and Treatment of Dyslipidemia by Ginsenoside Rb1
Jiaxin Wang, Nan Song, Qun Wang, Yuan Cao, Jie Wang, Yu Liu, Jingxuan Zhu, Xiaofei Sun, Lianqun JiaIntroduction:
This study employed combined transcriptomics and metabolomics analyses as well as experimental verification methods to comprehensively elucidate the molecular mechanism of ginsenoside Rb1 in preventing and treating dyslipidemia.
Methods:
First, a hyperlipidemia model was established using SPF-grade male SD rats, followed by an integrated analysis of metabolomics and transcriptomics. Subsequently, the target genes and metabolites identified through the multi-omics analysis were validated using experiments such as lipid assays, hematoxylin-eosin (HE) staining, Oil Red O staining, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analysis.
Results:
Metabolomic analysis revealed that 14 metabolites in the Rb1 group underwent alterations, involving pathways such as glycosylphosphatidylinositol (GPI) anchor biosynthesis, sphingolipid metabolism, and arachidonic acid metabolism. By integrating transcriptomic and metabolomic data, we identified 55 genes, including glucokinase (GCK) and phosphoglycerate mutase 1 (PGAM1), which are involved in glycolysis-related metabolic pathways and the regulation of glycolytic processes. Experimental results demonstrated that, compared with the model group, Rb1 administration significantly reduced the levels of glycolytic pathway enzymes, including GCK, PGAM1, GPI, PFKL, PGK, and LDHD, as well as associated metabolites. Simultaneously, the level of pyruvate carboxylase (ACC), a key enzyme in fatty acid synthesis, was also markedly decreased.
Discussion:
This study provides significant insights into research on dyslipidemia and offers new strategies and approaches for its clinical prevention and management.
Conclusion:
This suggests that Rb1 may affect fatty acid synthesis through the glycolytic pathway, thereby influencing dyslipidemia.