RESUMO
Putrescine and cadaverine are significant volatile indicators used to assess the degree of food spoilage. Herein, we propose a micro-nano multi cavity structure for surface-enhanced Raman spectroscopy (SERS) to analyze the volatile gas putrescine and cadaverine in decomposing food. The MoS2 nano-flowers are inserted into a PVDF micro-cavity through in-situ growth, followed by vacuum evaporation technology of Ag nanoparticles to form an Ag/MoS2 nano-flower cavity/PVDF micron-bowl cavity (FIB) substrate. The micro-nano multi cavity structure can improve the capture capacity of both light and gas, thereby exhibiting high sensitivity (EF = 7.71 × 107) and excellent capability for gas detection of 2-naphthalenethiol. The SERS detections of the putrescine and cadaverine are achieved in the spoiled pork samples with the FIB substrate. Therefore, this substrate can provide an efficient, accurate, and feasible method for the specific and quantitative detection in the food safety field.
RESUMO
BACKGROUND: The effective components contained in compound Kushen injection (CKI) and the genes and signalling pathways related to gastric cancer (GC) were analyzed through the network pharmacology method of traditional Chinese medicine, and various possible mechanisms by which CKI affects the proliferation, differentiation, survival, and metastasis of GC cells were discussed. The PI3K/AKT signalling pathway is considered to be one of the most important pathways targeted by CKI in the regulation of GC cells. The implementation of related cell experiments also confirmed the information we revealed. METHODS: Effective drug components of Kushen and Baituling in CKI were identified from the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). Genes related to GC were identified using the GENECARD and OMIM databases. The common target genes related to the effective components of the drug and GC were identified using the intersection method and visualized using software. A protein-protein interaction network (PPI) was established using STRING online software to confirm the key genes. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to predict the key pathways of CKI in GC treatment. BGC-803 and MKN-28 GC cells were used to verify the signalling pathway. Cell proliferation, apoptosis, migration ability, and invasion ability were assessed using CCK8, flow cytometry, scratch, and transwell assays. Immunofluorescence assays and western blotting were used to detect the expression of related proteins. RESULTS: CKI regulated GC cells through 35 effective drug components of GC-related target genes. In total, 194 genes were common targets of CKI and GC. The most significant function of the enriched genes was DNA-binding transcription activator activity as demonstrated by GO enrichment analysis. The metabolic pathway with the highest enrichment was the PI3K/AKT signalling pathway as demonstrated by KEGG enrichment analysis. Our cell experimental evidence also shows that CKI inhibits GC cell growth and migration and induce GC cell apoptosis. In addition, CKI inhibits the EMT process in GC cells through the PI3K/AKT signalling pathway. CONCLUSION: AKT1 is a key gene for CKI treatment of GC. CKI inhibited GC cell growth and migration and induced GC cell apoptosis. In addition, CKI regulated the EMT process in GC cells through the PI3K/AKT signalling pathway.