Solvation of the thiocyanate ion in three different deep eutectic solvents (DES) was investigated by linear FTIR spectroscopy, and Two Dimensional IR spectroscopy. Linear infrared spectroscopy reveals that the thiocyanate ion forms a hydrogen bond through its sulphur atom, while its nitrile end remains free. Photon-echo vibrational spectroscopy shows that the thiocyanate has a frequency-frequency correlation function (FFCF) with two distinct dynamics occurring on the picosecond time scale in all of the studied solvents. The observed dynamics is assigned to in-place and diffusional motions of the components within the thiocyanate solvation shell. Molecular dynamics simulations and ab initio calculations confirm the experimental findings and their molecular interpretation. In addition, theoretical modeling of the thiocyanate nitrile stretch lineshape suggests that alcohol-based DES are more structurally disorganized than the amide-based analogue. However, the organization observed in the different DES is not sufficient to explain physical properties, such as density, indicating that the amount of defects (i.e., hole theory) is not sufficient to fully describe the properties of DES.

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The aim of this study is to explore the apoptotic induction and cell cycle arrest function of luteolin on the liver cancer cells and the related mechanism. The liver cancer cell line SMMC-7721, BEL-7402, and normal liver cells HL-7702 were treated with different concentrations of luteolin. Cell proliferation ability was tested. Morphological changes of the apoptotic cells were observed under inverted fluorescence microscope after Hoechst33342 staining. We investigated the effect of luteolin on cell cycling and apoptosis with flow cytometry. The mitochondrial membrane potential changes were analyzed after JC-1 staining. Caspases-3 and Bcl-2 family proteins expression were analyzed by real-time PCR. Cell proliferation of SMMC-7721 and BEL-7402 were inhibited by luteolin, and the inhibition was dose-time-dependent. Luteolin could arrest the cells at G1/S stage, reduce mitochondrial membrane potential, and induce higher apoptosis rate and the typical apoptotic morphological changes of the liver carcinoma cells. Q-RT-PCR results also showed that luteolin increased Bax and caspase-3 expression significantly and upregulated Bcl-2 expression in a dose-dependent manner in liver carcinoma cells. However, the normal liver cells HL-7702 was almost not affected by luteolin treatment. Luteolin can inhibit SMMC-7721 and BEL-7402 cell proliferation in a time- and dose-dependent manner. And the mechanism maybe through arresting cell cycle at phase G1/S, enhancing Bax level, reducing anti-apoptotic protein Bcl-2 level, resulting in activating caspase-3 enzyme and decrease of mitochondrial membrane potential, and finally leading to cell apoptosis.

Circular RNA-microRNA (circRNA-miR) node has recently been found to modulate cancer process. Here, we investigated whether circCDYL and miR-150-5p exerted biological function in colon cancer cells. Colon cancer tissues were collected and subjected to qRT-PCR assay for circCDYL and miR-150-5p. SW480 and SW620 cells were forced to overexpress circCDYL and miR-150-5p before subjected to viability, colony formation, apoptosis, migration, invasion and protein (associated with proliferation, apoptosis and signaling pathways) assays. To confirm the combined function, the cells were transfected to simultaneously overexpress circCDYL and miR-150-5p. We found circCDYL was generally decreased while miR-150-5p was increased in colon cancer tissues in parallel with the para-carcinoma tissues. In circCDYL-transfected SW480 and SW620 cells, circ-CDYL decreased viability and promoted apoptosis with down-regulation of c-Myc and cyclin D1, up-regulation of p53, and cleavage of caspase-3 and PARP. Besides, migration and invasion behaviors were impeded. By contrast, miR-150-5p showed a carcinogenesis. However, suppressive role of circ-CDYL in cellular growth and migration was restrained in the cells simultaneously transfected with circCDYL and miR-150-5p, which was companied by down-regulation of PTEN and phosphorylation of PI3K, AKT, JAK2 and STAT5. circCDYL overexpression repressed cellular growth and migration via repressing miR-150-5p in colon cancer cells.

Positronium (Ps) formation cross sections (n = 1, 2) in positron-hydrogen collisions in Debye plasma environment are calculated using the screening approximation model for various Debye screening lengths from the Ps formation thresholds to 50 eV. The effect of the screened Coulomb potential on Ps formation process is investigated by using the Debye-Hückel potential. The present results are compared with available theoretical calculations.