We report a new fluorescent detection method for propofol based on graphene quantum dots (GQDs). Citric acid (CA) was selected as the carbon precursor, and fluorescent GQDs were prepared by carbonizing CA. The product, which efficiently quenched the fluorescence of GQDs, could be obtained through the oxidation of propofol in the presence of horseradish peroxidase and hydrogen peroxide. The fluorescence intensity ratio of GQDs (F/F0) was positively correlated with the concentration of propofol, which ranged within 5.34–89.07 mg l−1, the limit of detection was 0.5 mg l−1 and the limit of quantity was 5.34 mg l−1. The developed fluorescence method reported in the present study is simple, sensitive, reproducible, and can serve in determining propofol contents in emulsions.

BACKGROUND Polygoni Cuspidati Rhizoma et Radix (PCRR), a well-known traditional Chinese medicine (TCM), inhibits inflammation associated with various human diseases. However, the anti-inflammatory effects of PCRR in acute lung injury (ALI) and the underlying mechanisms of action remain unclear. AIM To determine the ingredients related to PCRR for treatment of ALI using multiple databases to obtain potential targets for fishing. METHODS Recognized and candidate active compounds for PCRR were obtained from Traditional Chinese Medicine Systems Pharmacology, STITCH, and PubMed databases. Target ALI databases were built using the Therapeutic Target, DrugBank, DisGeNET, Online Mendelian Inheritance in Man, and Genetic Association databases. Network pharmacology includes network construction, target prediction, topological feature analysis, and enrichment analysis. Bioinformatics resources from the Database for Annotation, Visualization and Integrated Discovery were utilized for gene ontology biological process and Kyoto Encyclopedia of Genes and Genomes network pathway enrichment analysis, and molecular docking techniques were adopted to verify the combination of major active ingredients and core targets. RESULTS Thirteen bioactive compounds corresponding to the 433 PCRR targets were identified. In addition, 128 genes were closely associated with ALI, 60 of which overlapped with PCRR targets and were considered therapeutically relevant. Functional enrichment analysis suggested that PCRR exerted its pharmacological effects in ALI by modulating multiple pathways, including the cell cycle, cell apoptosis, drug metabolism, inflammation, and immune modulation. Molecular docking results revealed a strong associative relationship between the active ingredient and core target. CONCLUSION PCRR alleviates ALI symptoms via molecular mechanisms predicted by network pharmacology. This study proposes a strategy to elucidate the mechanisms of TCM at the network pharmacology level.

No abstract

No abstract

Introduction: Usnic acid (UA) and barbatic acid (BA), two typical dibenzofurans and depsides in lichen, have a wide range of pharmacological activities and hepatotoxicity concerns. This study aimed to clarify the metabolic pathway of UA and BA and illuminate the relationship between metabolism and toxicity.Methods: An UPLC-Q-TOF-MS method was developed for metabolite identification of UA and BA in human liver microsomes (HLMs), rat liver microsomes (RLMs), and S9 fraction (RS9). The key metabolic enzymes responsible for UA and BA were identified by enzyme inhibitors combined with recombinant human cytochrome P450 (CYP450) enzymes. The cytotoxicity and metabolic toxicity mechanism of UA and BA were determined by the combination model of human primary hepatocytes and mouse 3T3 fibroblasts.Results: The hydroxylation, methylation, and glucuronidation reactions were involved in the metabolic profiles of UA and BA in RLMs, HLMs, and RS9. CYP2C9, CYP3A4, CYP2C8, and UGT1A1 are key metabolic enzymes responsible for metabolites of UA and CYP2C8, CYP2C9, CYP2C19, CYP1A1, UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, and UGT1A10 for metabolites of BA. UA and BA did not display evident cytotoxicity in human primary hepatocytes at concentrations of 0.01–25 and 0.01–100 µM, respectively, but showed potential cytotoxicity to mouse 3T3 fibroblasts with 50% inhibitory concentration values of 7.40 and 60.2 µM.Discussion: In conclusion, the attenuated cytotoxicity of BA is associated with metabolism, and UGTs may be the key metabolic detoxification enzymes. The cytotoxicity of UA may be associated with chronic toxicity. The present results provide important insights into the understanding of the biotransformation behavior and metabolic detoxification of UA and BA.