Gnaphalium hypoleucum DC. was first recorded in the Chinese National Pharmacopoeia “Yi Plant Medicine”. There is no detailed report on its main components’ activity in suppressing the quorum sensing activity (QS) of bacteria. Our study aimed to screen the main components in extracts of G. hypoleucum DC. in order to measure their effects on bacterial QS activity and to explore specific quorum sensing mechanisms that are affected by G. hypoleucum DC. extracts. Crude extracts of G. hypoleucum DC. contained significant amounts of two compounds shown to inhibit bacterial QS activity, namely apigenin and luteolin. Apigenin and luteolin in crude extracts of G. hypoleucum DC. showed substantial inhibition of pigment formation, biofilm production, and motility in Chromobacterium violaceum ATCC 12472 compared to the effects of other phytochemicals from G. hypoleucum DC. Apigenin and luteolin exhibited a strong QS inhibitory effect on C. violaceum, interfering with the violacein pigment biosynthesis by downregulating the vioB, vioC, and vioD genes. In the presence of signal molecules, the QS effect is prevented, and the selected compounds can still inhibit the production of the characteristic purple pigment in C. violaceum. Based on qualitative and quantitative research using genomics and bioinformatics, we concluded that apigenin and luteolin in crude extracts of G. hypoleucum DC can interfere with the generation of QS in C. violaceum by downregulating the vioB, vioC, and vioD genes. Indeed, G. hypoleucum DC. is used for the treatment of bacterial infections, and this research provides new ideas and potential alternative uses for medicinal plants.

The aim of this study is to advance the application of network toxicology, AlphaFold 3 and molecular docking techniques in the toxicity analysis of heavy metal ions (HMIs) and heavy metal ions organic complexes (HMIOCs) in environmental pollutants. In this study, the potential toxicity and molecular mechanisms of HMIs and HMIOCs in environmental pollutants were effectively investigated using Cobalt(II) ion & Bis-(2,4-pentanedionato)cobalt(II) (Co(II) & BPCo(II)) as examples. It was found that Co(II) & BPCo(II) regulates multiple signaling pathways by modulating hub targets such as APP, NR3C1, ESR1, CASP3, MMP9, and PTGS2. These pathways include Serotonergic synapse, Cocaine addiction, Pathways of neurodegeneration-multiple diseases, Calcium signaling pathway, Neuroactive ligand-receptor interactions, Alzheimer disease and other pathways, which in turn affects the Blood-Brain Barrier (BBB) in order to destroy neuronal cells, ultimately leading to a variety of mental illnesses (MIs) and nervous system diseases (NSDs), such as Schizophrenia, Depressive disorder, nervous system disorder and Alzheimer Disease, Late Onset. In this study, the toxic effects and molecular mechanisms of Co(II) and BPCo(II) were elucidated, while the limitations of conventional toxicological methods—such as safety issues, time constraints, high expenses, ethical concerns regarding animal use, and limited predictive power—were effectively addressed. These results contribute to the foundation for studying disease diagnosis associated with environmental exposure to HMIs and HMIOCs. Graphical