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Background Geraniol is an acyclic monoterpene alcohol, which is extracted from the ethereal oils of aromatic plants. A systematic analysis of its mechanism of action has not yet been carried out. Methods In this study, the druggability of geraniol was assessed via Traditional Chinese Medicine Systems Pharmacology Database (TCMSP), and the potential targets of geraniol were identified using the Comparative Toxicogenomics Database (CTD). Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using WebGestalt. Drug-target-pathway networks were constructed using Cytoscape to give a visual view. Results Our findings showed that geraniol has superb druggability with 38 putative identified target genes. GO, KEGG, and network analyses revealed that these targets were associated with cancer, inflammatory immunoreactions, and other physiological processes. Conclusion Geraniol is predicted to target multiple proteins and pathways that shape a network which can exert systematic pharmacological effects.

Background: Fetal growth restriction (FGR) is a worldwide problem, and a major cause of perinatal morbidity. The precise molecular mechanisms involved in placental development and function during FGR remain poorly understood. Circular RNAs (circRNAs) are important biological molecules associated with disease pathogenesis. However, the role of circRNAs in FGR has not been well studied. Methods: circRNA expression profiles in placental tissues with and without FGR were identified by circRNA microarray. circRNA expression was verified by quantitative reverse-transcription PCR (RT-qPCR) assay. The effect of hsa_circ_0000848 and hsa-miR-6768-5p on HTR-8 cell apoptosis, migration, and invasion was evaluated. The association between hsa_circ_0000848 and hsa-miR-6768-5p was confirmed by dual luciferase activity and anti-AGO2 RNA immunoprecipitation (RIP) assays. Protein levels were examined via western blotting. Results: RT-qPCR results showed that hsa_circ_0000848 expression was significantly down-regulated in FGR placenta. Hsa_circ_0000848 overexpression and hsa-miR-6768-5p inhibitor suppressed apoptosis, and promoted cell migration and invasion. In addition, hsa_circ_0000848 overexpression and hsa-miR-6768-5p inhibitor increased the protein abundance of BCL2, MMP2 and MMP9, and decreased the protein abundance of cleaved caspase-3, cleaved caspase-9, and BAX, whereas hsa_circ_0000848 knockdown caused the opposite effect. Moreover, a significant increase in hsa-miR-6768-5p expression and a negative correlation between hsa_circ_0000848 and hsa-miR-6768-5p were identified in the FGR tissues. Luciferase reporter and RIP assay results revealed binding of hsa-miR-6768-5p to hsa_circ_0000848. Furthermore, hsa-miR-6768-5p overexpression eliminated the effect of hsa_circ_0000848 overexpression in HTR-8 cells.