A new electrochemical sensor for organophosphate pesticide(methyl-paraoxon)detection based on bifunctional cerium oxide(CeO2)nanozyme is here reported for the first time.Methyl-paraoxon was degraded into p-nitrophenol by using CeO2 with phosphatase mimicking activity.The CeO2 nanozyme-modified electrode was then synthesized to detect p-nitrophenol.Cyclic voltammetry was applied to investigate the electrochemical behavior of the modified electrode,which indicates that the signal enhancement effect may attribute to the coating of CeO2 nanozyme.The current research also studied and discussed the main parameters affecting the analytical signal,including accumulation potential,accumulation time,and pH.Under the optimum conditions,the present method provided a wider linear range from 0.1 to 100 μmol/L for methyl-paraoxon with a detection limit of 0.06 μmol/L.To validate the proof of concept,the electrochemical sensor was then successfully applied for the determination of methyl-paraoxon in three herb samples,i.e.,Coix lacryma-jobi,Adenophora stricta and Semen nelum-binis.Our findings may provide new insights into the application of bifunctional nanozyme in electro-chemical detection of organophosphorus pesticide.

Objective    To investigate the effects of telmisartan on the proliferation, migration and apoptosis of non-small cell lung cancer A549 and the mechanism of regulating Wnt signaling pathway. Methods    Non-small cell lung cancer cell line A549 was cultured in vitro. Cell counting kit-8 (CCK-8) assay was used to detect the effect of telmisartan at different concentrations on the proliferative activity of A549 cells. The survival fraction of A549 treated with different concentrations of telmisartan was determined by colony-formation assay. The effect of telmisartan at different concentrations on the migration ability of A549 cells was examined in the wounding healing assay. Hoechst staining was used to detect the effects of telmisartan at different concentrations on the apoptosis of A549. Western bloting was used to detect the expressions of β-actin, proliferating cell nuclear antigen (PCNA), Bax, Bcl-2, Wnt-3a, Beta-catenin (β-catenin), serine protein kinase 3β (p-GSK-3β), glycogen synthase kinase-3β (GSK-3β) and c-myc. Results    Different concentrations of telmisartan treatment inhibited the proliferation activity, colony-formation rate and migration of A549 cells, and reduced the expression of PCNA in a concentration-dependent manner. Telmisartan treatment promoted the apoptosis of A549 cells, significantly increased the expression of pro-apoptotic protein Bax and decreased the expression of anti-apoptotic protein Bcl-2. The expression levels of Wnt-3a, β-catenin, p-GSK-3β, and c-myc in A549 cells increased after treatment with telmisartan, while the expression levels of GSK-3β decreased. Conclusion    Telmisartan may play a role in the proliferation, migration and apoptosis of non-small cell lung cancer A549 cells, and  inhibiting the Wnt/β-catenin signaling pathway may be one of the mechanisms.

AIM: To study the pharmacokinetics (PK) of pazopanib tablets and explore the genetic mechanism of individual differences in drug metabolism primarily. METHODS: Fourteen healthy male subjects were respectively administrated with a single dose pazopanib tablet (200 mg) orally on the day of dosing, and their blood samples were collected from baseline to 96 hours. The serum concentration of pazopanib was measured by LC-MS/MS, the parameters of PK were calculated by winnonlin 6.3 software, and the gene polymorphism of cytochrome P450 3A4 (CYP3A4) was determined by snapshot method. RESULTS: The range of C