Objective To study the best preparation technique of compound Thallus laminaria granules volatile oil-?-cyclodextrin clathrate and examine the stability of the elathrate.Methods The orthogonal design method was used to optimize the formulation.The yeild of the volatile oil and the content of the clathrate were used as the test target.Results The best preparation process was as follows:?-cyclodextrin:compound Thallus laminaria=12:1(g?mL~(-1)),at 50～60℃for 2 hours.Making distillation twice while adding water to the first decoction, steaming 1h after boiling;A_2 B_1 was the best extraction scheme.Conclusion The preparation process can be a scheme to obtain the clathrate with high content of effective component,which can be used in the preparation of the clathrate.

PURPOSE: Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been deemed an oncogene in many human cancers. However, the underlying mechanism of NEAT1 in nasopharyngeal carcinoma (NPC) progression remains largely unclear. MATERIALS AND METHODS: Quantitative real-time PCR assay was performed to assess the expression of NEAT1 and miR-34a-5p in NPC tissues and cells. Western blot analysis was used to observe cell epithelial to mesenchymal transition (EMT) and the activation of Wnt/β-catenin signaling in 5-8F cells. MiRNA directly interacting with NEAT1 were verified by dual-luciferase reporter assay and RNA immunoprecipitation. Cell proliferation ability was determined by CCK-8 assay, and cell migration and invasion capacities were assessed by transwell assays. An animal model was used to investigate the regulatory effect of NEAT1 on tumor growth in vivo. RESULTS: Our data revealed that NEAT1 is upregulated, while miR-34a-5p is downregulated in NPC tissues and cell lines. NEAT1 knockdown repressed tumor growth in vitro and in vivo. Additionally, we discovered that NEAT1 directly binds to miR-34a-5p and suppresses miR-34a-5p expression. Moreover, NEAT1 knockdown exerted suppression effects on cell proliferation, migration, invasion, and EMT by miR-34a-5p. NEAT1 knockdown blocked Wnt/β-catenin signaling via miR-34a-5p. CONCLUSION: Our study demonstrated that NEAT1 targets miR-34a-5p at least partly to drive NPC progression by regulating Wnt/β-catenin signaling, suggesting a potential therapeutic target for NPC.
Blotting, Western ; Cell Line ; Cell Movement ; Cell Proliferation ; Humans ; Immunoprecipitation ; In Vitro Techniques ; MicroRNAs ; Models, Animal ; Oncogenes ; Real-Time Polymerase Chain Reaction ; RNA ; RNA, Long Noncoding ; Sincalide