Network Pharmacology-based Mechanism of Xiao Xianxiongtang in Treatment of Coronary Heart Disease
Objective; To predict Xiao Xianxiongtang s treatment of coronary heart disease (CHD) targets and analyze their function by the network pharmacology method, and build ingredients-targets-channel network pharmacological model, in order to reveal potential pathways and mechanisms of Xiao Xianxiongtang for CHD treatment. Method; Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) was used to obtain components, and CHD targets over Xiao Xianxiongtang were predicted by using Swiss Target Prediction reverse pharmacophore matching method. CHD targets which Food and Drug Administration (FDA) approved were collected from Therapeutic Target Database (TTD) , Drugbank and Disease-gene Net databases (DisGeNET) . Wenn diagram was used to obtain the correlation intersection. Target characteristics were analyzed with GE02R online, Reactome FI was used to analyze the enrichment of target pathways, and Cytoscape software was used to construct the " component-target-pathway" network. Result: Network analysis showed that Xiao Xianxiongtang treated CHD by regulating 24 target proteins through 25 therapeutic components, and acting on 21 specific pathways and 4 biological processes. According to the multiple gene chip analysis of GE02R online, there were up-down-regulated differences in the targets, including 11 up targets and 13 down targets. Conclusion: Xiao Xianxiongtang treats CHD by involving the biological processes through berberine and flavonoid groups of Coptidis Rhizoma, nucleosides and organic acids of Arum ternatum Thunb, stigmasterols and flavonoids of Trichosanthes kirilowii Maxim, such as gene expression, metabolism and protein metabolism, adjusting the gene expressions of relevant target proteins, regulating gene transcription pathways, such as biological oxidation reaction and lipid and lipoprotein metabolism, insulin-like growth factor binding protein (IGFBPs) of insulin-like growth factor (IGF) transshipment and intake, and the degradation of extracellular matrix signaling pathways.
