Frontiers in pharmacology · 2026
Integrating multi-omics and deep learning to explore the active ingredients and molecular mechanisms of Cinnamomum migao volatile oil in the treatment of coronary heart disease.
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Zeng Xiaomei, Guo Jiangtao, Xu Jian, Zhang Yongping, Zhu Xiaoting, Liu Jie
Аннотация
BACKGROUND: Coronary heart disease (CHD) is a major cardiovascular disease. Cinnamomum migao volatile oil (CM-VO) is traditionally used for CHD, but its active basis and mechanisms remain unclear.
OBJECTIVE: To clarify the chemical basis and potential anti-CHD mechanisms of CM-VO.
METHODS: GC-MS was used to identify CM-VO constituents and serum-related metabolites. A mouse CHD model was established to evaluate pharmacodynamic effects. Network analysis was used for full-component mechanism prediction, while transcriptomics was used to screen treatment-responsive genes. UniProt standardization, deep learning, molecular docking, and H9c2 cell experiments were further performed for target prediction and validation.
RESULTS: A total of 68 CM-VO constituents and 8 serum-related metabolites were identified. CM-VO improved myocardial injury, inflammation, oxidative stress, endothelial dysfunction, and lipid-related abnormalities in CHD mice. Network analysis predicted 39 bioactive compounds and 58 key targets, while transcriptomics identified 44 DEGs and 101 CHD-related enriched genes. After UniProt standardization, 19 human genes were analyzed, and GADD45A, MTHFS, and ALAS2 were prioritized as high-affinity targets. In H9c2 cells, CM-VO-containing serum reduced lipid accumulation and injury markers, enhanced antioxidant capacity, and regulated GADD45A, MTHFS, and ALAS2 expression.
CONCLUSION: CM-VO may protect against CHD mainly by regulating inflammation, oxidative stress, endothelial function, and lipid metabolism. This study provides integrated evidence for the pharmacological basis and molecular mechanisms of CM-VO against CHD.
OBJECTIVE: To clarify the chemical basis and potential anti-CHD mechanisms of CM-VO.
METHODS: GC-MS was used to identify CM-VO constituents and serum-related metabolites. A mouse CHD model was established to evaluate pharmacodynamic effects. Network analysis was used for full-component mechanism prediction, while transcriptomics was used to screen treatment-responsive genes. UniProt standardization, deep learning, molecular docking, and H9c2 cell experiments were further performed for target prediction and validation.
RESULTS: A total of 68 CM-VO constituents and 8 serum-related metabolites were identified. CM-VO improved myocardial injury, inflammation, oxidative stress, endothelial dysfunction, and lipid-related abnormalities in CHD mice. Network analysis predicted 39 bioactive compounds and 58 key targets, while transcriptomics identified 44 DEGs and 101 CHD-related enriched genes. After UniProt standardization, 19 human genes were analyzed, and GADD45A, MTHFS, and ALAS2 were prioritized as high-affinity targets. In H9c2 cells, CM-VO-containing serum reduced lipid accumulation and injury markers, enhanced antioxidant capacity, and regulated GADD45A, MTHFS, and ALAS2 expression.
CONCLUSION: CM-VO may protect against CHD mainly by regulating inflammation, oxidative stress, endothelial function, and lipid metabolism. This study provides integrated evidence for the pharmacological basis and molecular mechanisms of CM-VO against CHD.