Dissipation Behavior of Three Fungicides during the Industrial Processing of PaeoniaeRadix Alba and Associated Processing Factors.

Before being administered as medicinal products, Chinese herbal medicines (CHMs) must be processed and decocted for human consumption. While the presence of pesticide residues in CHMs is a major concern, pesticide dissipation behavior during CHM processing has rarely been reported. In this study, the dissipation of three pesticide residues in the CHM Paeoniae Radix Alba (PRA) was investigated during each step of industrial processing. The boiling process was found to significantly reduce pesticide residues (61-89%), and the peeling process also contributed to pesticide degradation (29-68%). The high temperature (60 °C) during the drying process led to further pesticide degradation. The processing factors of all three pesticides after each processing step were less than one, and the processing factors for the overall process were lower than 0.027, indicating that industrial processing clearly reduced the amount of pesticide residues (97.3-99.4%). The findings provide guidance for the safe use of fungicides in CHMs and can help establish maximum residue limits for PRA to reduce human exposure to pesticides.

Structure Identification and In Vitro Anticancer Activity of Lathyrol-3-phenylacetate-5,15-diacetate.

Natural products from the genus Euphorbia show attention-attracting activities, such as anticancer activity. In this article, classical isolation and structure identification were used in a study on Caper Euphorbia Seed. Subsequently, MTT and wound healing assays, flow cytometry, western blotting, Hoechst 33258 staining and fluorescence microscopy examination were applied to investigate the anticancer activity of the obtained compounds. In a result, lathyrol-3-phenyl- acetate-5,15-diacetate (deoxy Euphorbia factor L1, DEFL1) was isolated from Caper Euphorbia Seed. Moreover, the NMR signals were totally assigned. DEFL1 showed potent inhibition against lung cancer A549 cells, with an IC50 value of 17.51 ± 0.85 µM. Furthermore, DEFL1 suppressed wound healing of A549 cells in a concentration-dependent manner. Mechanically, DEFL1 induced apoptosis, with involvement of an increase of reactive oxygen species (ROS), decrease of mitochondrial membrane potential (ΔΨm), release of cytochrome c, activity raise of caspase-9 and 3. Characteristic features of apoptosis were observed by fluorescence microscopy. In summary, DEFL1 inhibited growth and induced apoptosis in lung cancer A549 cells via a mitochondrial pathway.