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Background: Cholangiocarcinoma (CCA) is a rare biliary adenocarcinoma related to poor clinical prognosis. Crowberry is an herbal medicine used to control inflammatory diseases and reestablish antioxidant enzyme activity. Although crowberry shows significant therapeutic efficacy in various tumors and diseases, its anticancer effects and specific molecular mechanisms in CCA are poorly understood. Aim of the study: This study was conducted to characterize crowberry effects on CCA cells behavior. Materials and methods: The chemical profiles of crowberry extract was qualitatively analyzed by high-performance liquid chromatography (HPLC) and HPLC–tandem mass spectrometry. MTT, colony formation and EdU assays were performed to measure cell proliferation. The effect of crowberry treatment on CCA cell migration was assessed by wound healing and migration assays. Moreover, Hoechst staining assay and flow cytometry were performed to assess the cell apoptosis rate. Western blotting was used to assess the protein expression levels of key factors associated with apoptosis, the Akt signaling pathway, and the epithelial-mesenchymal transition. A xenograft model was established and immunohistochemical and H&E staining was performed to assess crowberry antitumor effects in vivo. Results: Crowberry clearly inhibited CCA cells proliferation and migration in a dose-dependent manner and induced apoptosis in vitro. Crowberry inactivated the PI3K/Akt signaling pathway by regulating DEK in vitro and significantly inhibited tumor growth by downregulating the DEK expression in xenograft models. Conclusion: Crowberry inhibits CCA cells proliferation and migration through a molecular mechanism that includes inhibition of DEK and Akt signaling pathway inhibition in vitro and in vivo. Highlights: Crowberry alterd expression levels of key mediators in PI3K/Akt signaling pathway. Crowberry alterd expression levels of key mediators in PI3K/Akt signaling pathway. Crowberry suppressed the expression of the proto-oncogene DEK in vivo and in vitro. Crowberry inhibited CCA progression and migration through a molecular mechanism that includes inhibition of DEK and the Akt signaling pathway in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Phthalimide can be formed from either the degradation of folpet and phosmet, or reaction of phthalic anhydride with primary amino groups. Consequently, the sum of phthalimide and folpet, expressed as folpet‐residue definition, is highly prone to false‐positive levels of folpet in tea. An analytical method is thus urgently needed to investigate the residue level and source of phthalimide in tea. In this work, we developed an accurate method of determining phthalimide and phthalic acid (the indicator of phthalic anhydride) by acetonitrile extraction and 3‐bromopropyltrimethylammonium bromide derivatization coupled with ultra high performance liquid chromatography and high‐resolution mass spectrometry. The method was validated, and linearity (correlation coefficients > 0.99) was obtained. Satisfactory recoveries at 10, 20, 50, and 100 μg/kg ranged from 76 to 117%, and the intra‐ and interday accuracies were <23%. The limit of quantification for phthalimide and phthalic acid was 10 μg/kg. The developed method was further successfully used to determine phthalimide and phthalic acid in some tea samples. The positive rate of phthalimide and phthalic acid detected in the tea samples ranged from 30–75 and 50–90%, respectively. [ABSTRACT FROM AUTHOR]

DOI: 10.1002/jssc.201801128 The cover picture shows an accurate method of determining phthalimide (PI) and phthalic acid (PA) in tea by acetonitrile extraction and 3‐bromopropyltrimethylammonium bromide derivatization coupled with ultraperformance liquid chromatography high resolution mass spectrometry. The method was validated, and satisfactory linearity, recovery, repeatability values were obtained. Then, the developed method was further successfully used to determine PI and PA in different tea matrices. All these observations provided crucial information and an analytical method to further study the sources and the related pathway of PI generation in tea. [ABSTRACT FROM AUTHOR]

• A novel method for simultaneous determination of 38 PCBs in tea using GC–MS/MS. • D-SPE combined with PVPP adsorbent effectively removed tea matrices. • Satisfactory sensitivity and recovery were obtained for most PCBs. • Different tea samples (green, oolong and black tea) were analyzed. A gas chromatography–tandem mass spectrometry method was developed for simultaneous determination of 38 polychlorinated biphenyls (PCBs) in tea. Sample preparation was based on a dispersive solid phase extraction procedure through an extraction of target compounds. An appropriate amount of polyvinylpolypyrrolidone was directly added in tea extractions to effectively remove polyphenols, and then tea extracts were cleaned up with primary secondary amine, florisil and graphitised carbon black. The method was validated, and linearity with correlation coefficients higher than 0.99 was obtained. Satisfactory recoveries at 2, 10, 50, and 100 µg kg−1 ranged from 71% to 117% with a maximum relative standard deviation of 23%, except for PCB 81, 77, 126 and 169, of which recoveries were in the range of 32%–63%. Limits of quantitation for PCBs were 2 or 10 µg kg−1, which was set as the lowest validated and spiked level meeting the acceptable accuracy and precision. [ABSTRACT FROM AUTHOR]