Affiliation:
1. Department of Laboratory Medicine The First Medical Center of Chinese PLA General Hospital Beijing China
2. Medical School of Chinese PLA Beijing China
3. Shanghai Jiao Tong University Shanghai China
4. School of Laboratory Medicine Weifang Medical College Weifang Shandong China
Abstract
AbstractBackgroundA combination of molecular docking, molecular dynamics simulations, and herbal network pharmacology was used to investigate the shared key targets and potential mechanisms underlying the preventive effects of Ginkgo biloba active compounds against acute mountain sickness (AMS) and ischemic stroke (IS).Material and MethodsThe Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform was used to screen the main active compounds of Ginkgo biloba and their corresponding targets. We obtained AMS‐related genes by mining several databases and cross‐correlated them with key active compounds of Ginkgo biloba to identify relevant action targets for treating AMS. The STRING database was used to construct a protein–protein interaction network of the effect of Ginkgo biloba active compounds on AMS targets. The expression of genes in the network was analyzed in an IS dataset to identify common key targets of Ginkgo biloba active compounds for both AMS and IS prevention.ResultsThe intersection between the targets of Ginkgo biloba active compounds and AMS‐related genes identified 43 overlapping genes. Analysis of the protein–protein interaction network showed that VEGFA, TP53, SERPINE1, and PTGS2 were among the key hub genes. Analysis of the IS dataset identified significant differences in the expression levels of CAT, TP53, CXCL8, NFKBIA, and PTGS2. These genes were used to construct a visual nomogram prediction model for IS prognosis with promising clinical implications. Molecular docking and molecular dynamics simulations indicated that sesamin stably targeted and bound to PTGS2.ConclusionsActive ingredients of Ginkgo biloba, including luteolin, quercetin, and sesamin, have the potential to modulate the development of AMS and IS through targeted interactions with key proteins, including TP53, CXCL8, NFKBIA, PTGS2, and CAT.