OBJECTIVE To explore the mechanism of action of active components of Nostoc commune in anti-triple-negative breast cancer(TNBC) by the network pharmacology method and molecular biology experiment. METHODS The active components of Nostoc commune were collected by consulting the literature and combined with the preliminary research in the laboratory, the Swiss Target Prediction database was used for target prediction, and the disease targets were obtained in the TTD, Genecards and OMIM databases. The STRING online platform was used for protein-protein interaction, and the KEGG signaling pathway and GO gene function enrichment analysis were performed using the Metascape database. Molecular docking of N-acetyltryptamine, a component of Nostoc commune, and target AKT1 by AutoDock software. Annexin V-FITC/PI double staining method was performed to analyze the apoptotic rate of cells. RT-qPCR and Western blotting were used to detect the mechanism of action of the active components of Nostoc commune on anti-TNBC. RESULTS The results of network pharmacology showed that there were 8 effective components, such as N-acetyltryptamine, Scytonemin and Nostocionone, involved 75 key targets such as signal transduction and AKT1, STAT3 and CCND1. The KEGG signaling pathway and GO gene function enrichment analysis results involved cancer-related signaling pathways, PI3K-Akt signaling pathways and MAPK signaling pathways. Molecular docking showed that N-acetyltryptamine had better affinity with AKT1. N-acetyltryptamine could not significantly promote apoptosis of breast cancer cells. Western blotting showed that N-acetyltryptamine could down-regulate the protein expressions of AKT1. The results of RT-qPCR showed that N-acetyltryptamine could effectively reduce the mRNA expression of AKT1 in cells. CONCLUSION N-acetyltryptamine may inhibit the proliferation of TNBC cells by inhibiting the AKT1 signaling pathway, thereby exerting anti-TNBC effects.

OBJECTIVE To observe the effects of sodium p-hydroxybenzoate on the central nervous system and cardiovascular system of experimental animals. METHODS Kunming mice were given a single dose of sodium p-hydroxybenzoate of 20, 50 and 100 mg·kg-1 by oral gavage, the effects of sodium p-hydroxybenzoate on the central nervous system were observed by mice tail-flick experiment, mice autonomic activity experiment, pole-climbing experiment, coordinating hypnosis test and Morris water maze experiment. SD rats were given a single dose of sodium p-hydroxybenzoate of 14, 35 and 70 mg·kg-1 and Beagle dogs were given a single dose of sodium p-hydroxybenzoate of 4.2, 10.5 and 21 mg·kg-1 by oral gavage, the effects of sodium p-hydroxybenzoate on cardiovascular system and body temperature were observed by measuring blood pressure and body temperature in Beagle dogs, and measuring electrocardiogram in SD rats. RESULTS There was no significant influence of sodium p-hydroxybenzoate on sensory-motor reflex, autonomic activity, coordinated movements, sleep rate of mice with the sub-threshold sleep dose of pentobarbital sodium and learning-memory ability. Similarly, there were no significant effects on electrocardiogram of SD rats and there were no significant effects on blood pressure and body temperature of Beagle dogs. CONCLUSION Single oral gavage of sodium p-hydroxybenzoate has no significant effects on the cardiovascular system and the central nervous system of experimental animal under the condition.