Analysis of the Mechanism of Maslinic Acid on Papillary Thyroid Carcinoma Based on RNA-Seq Technology.

Objective: This study analyzed gene sequence changes in the thyroid papillary carcinoma (PTC) cell line TPC-1 treated with the natural compound maslinic acid (MA) through RNA-sequencing (RNA-seq) and identified the necessary genes to provide a basis for the study of the molecular mechanism of action of MA in PTC treatment. Methods: RNA-seq technology was used to detect genetic differences between the normal cell group (Nthy-ori 3-1) and the TPC-1 cell group (N vs T). Then, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, Venn diagram analysis of shared genes, and protein-protein interaction (PPI) network analysis were used to analyze the therapeutic effect of the MA on TPC-1 cells. Real-time quantitative PCR (qRT-PCR) was used to verify six key genes. Results: GO and KEGG analyses showed that four crucial signaling pathways are related to TPC development: cytoplasmic molecule (cell adhesion molecules), neuroactive ligand-receptor interaction, tumor transcriptional disorder, and cytokine-cytokine interaction. The Venn diagram revealed 434 genes were shared between the MA vs T-group and 387 genes were shared between the MATH vs T and N vs T groups. PPI and ClueGO showed that NLRP3, SERPINE1, CD74, EDN1, HMOX1, and CXCL1 genes were significantly associated with PTC, while CXCL1, HMOX1, and other factors were mainly involved in the cytokine-cytokine interaction. The qRT-PCR results showed that the expression of NLRP3, EDN1, HMOX1, and CXCL1 genes was significantly upregulated in the TPC-1 group but significantly downregulated after MA treatment (p < 0.01). SERPINE1 and CD74 genes were not expressed in TPC-1 cells, whereas they were significantly upregulated after MA treatment (p < 0.01). Conclusions: This present study proves for the first time that MA can treat PTC, and the preliminary identification of key genes and rich signal transduction pathways provides potential biomarkers. It also provides potential biomarkers for the treatment of PTC with the natural compound MA and preliminarily discusses the therapeutic mechanism of action of MA against PTC, which is helpful for the further diagnosis and treatment of PTC patients.

Experimental Study on the Effect of Tibetan Medicine Triphala on the Proliferation and Apoptosis of Pancreatic Islet ß Cells through Incretin-cAMP Signaling Pathway.

According to the data, there are 387 million people with diabetes in the world, and the number of people with diabetes is expected to reach 600 million by 2035 (Nature Reviews Endocrinology, 14, 2018, Zheng et al.). At present, there are nearly 110 million diabetic patients in China, the incidence of which is increasing (Diabetologia, 61, 2018, Ma). Islet ß cell apoptosis and proliferation is an important basis for the occurrence and development of diabetes. It has been reported that enhancing the activity of incretin-cAMP signaling pathway can also promote islet ß cell proliferation, reduce ß cell apoptosis and promote insulin secretion (Diabetologia, 59, 2016, Iida et al.). Tibetan medicine Triphala (THL) is a traditional national medicine, it plays a good role in anti-fatigue, antioxidation, prevention and treatment of polycythemia at high altitude. Research have shown that it can reduce blood glucose in patients with diabetes and inhibit the activity of glucosidase in the intestines (The Journal of Alternative and Complementary Medicine, 23, 2017, Peterson et al.). After the diabetic Wistar rat model induced by Streptozocin (STZ) was successfully duplicated, the positive drug sitagliptin tablet and THL were given and the changes of body weight and blood glucose were measured. After 6 weeks, the expression of related factors in serum and pancreas was observed. Compared with the model group, in the treatment group, blood glucose decreased, body weight increased, incretin-cAMP signaling pathway related factors glucose-dependent insulin-promoting polypeptide (GIP), glucagon-like peptide-1 (GLP-1), GLP-1R, cAMP, P-protein kinase A (PKA), AKT were up-regulated, insulin secretion was increased, liporing protein interaction protein (TXNIP) expression was down-regulated. In addition, in the treatment group, the degree of islet atrophy was alleviated and the number of islet ß cells increased. This study shows that THL may enhance the activity of incretin-cAMP signal pathway and affect the proliferation and apoptosis of islet ß cells, so as to achieve the effect of anti-diabetes.

[Study of tyrosine online fluorescence spectrum under high pressure].

The effect of pressure on fluorescence of tyrosine (Tyr) and Tyr in different concentration of Cu2+ was investigated. The results showed that Tyr fluorescence intensity was enhanced with increasing pressure in the absence of Cu2+, with the fluorescence intensity increasing by about 9% when the pressure reached 60 MPa. Furthermore, Tyr fluorescence quenched by Cu2+ and the quenching became stronger when the concentration of Cu2+ was higher. The effect of pressure on the fluorescence of Tyr was different under various Cu2+ concentrations. When Cu2+ concentration was lower, the fluorescence intensity increased relatively weakly (under 60 MPa and [Copper ion]/[Tyr] = 1, fluorescence intensity increased by 14.4%) and vice versa, the fluorescence intensity increased relatively strongly (under 60 MPa and [Copper ion]/[Tyr] = 40, fluorescence intensity increased by 38.4%).