An Efficient Deacidification Process for Safflower Seed Oil with High Nutritional Property through Optimized Ultrasonic-Assisted Technology.

Safflower seed oil (SSO) is considered to be an excellent edible oil since it contains abundant essential unsaturated fatty acids and lipid concomitants. However, the traditional alkali-refined deacidification process of SSO results in a serious loss of bioactive components of the oil and also yields massive amounts of wastewater. In this study, SSO was first extracted by ultrasonic-assisted ethanol extraction (UAEE), and the extraction process was optimized using random centroid optimization. By exploring the effects of ethanol concentration, solid−liquid ratio, ultrasonic time, and the number of deacidification times, the optimum conditions for the deacidification of safflower seed oil were obtained as follows: ethanol concentration 100%, solid−liquid ratio 1:4, ultrasonic time 29 min, and number of deacidification cycles (×2). The deacidification rate was 97.13% ± 0.70%, better than alkali-refining (72.16% ± 0.13%). The values of acid, peroxide, anisidine and total oxidation of UAEE-deacidified SSO were significantly lower than those of alkali-deacidified SSO (p < 0.05). The contents of the main lipid concomitants such as tocopherols, polyphenols, and phytosterols in UAEE-decidified SSO were significantly higher than those of the latter (p < 0.05). For instance, the DPPH radical scavenging capacity of UAEE-processed SSO was significantly higher than that of alkali refining (p < 0.05). The Pearson bivariate correlation analysis before and after the deacidification process demonstrated that the three main lipid concomitants in SSO were negatively correlated with the index of peroxide, anisidine, and total oxidation values. The purpose of this study was to provide an alternative method for the deacidification of SSO that can effectively remove free fatty acids while maintaining the nutritional characteristics, physicochemical properties, and antioxidant capacity of SSO.

Downregulation of TRIM28 inhibits growth and increases apoptosis of nude mice with non­small cell lung cancer xenografts.

TRIM28 is a well­known transcriptional co­repressor of Kruppel­associated box zinc finger proteins. The authors previously demonstrated that TRIM28 small interfering (si)RNA decreases cell proliferation and inhibits cell cycle progression in non­small cell lung cancer (NSCLC) cell lines. The present study further demonstrated that the stable silencing of TRIM28 expression by a specific siRNA lentivirus vector significantly inhibited the growth and exerted obvious anti­tumor effects in nude mice. The results of the terminal deoxynucleotidyl transferase­mediated deoxyuridine triphosphate nick­end labeling assay indicated that TRIM28 knockdown increased apoptosis. Furthermore, TRIM28 knockdown decreased the expression of B cell lymphoma (Bcl)­2 and increased the expression of Bcl­2 associated X, apoptosis regulator and p53 at the gene and protein levels. Auto­antibodies to TRIM28 were present in 12.32% of the sera of the patients with NSCLC. The results suggest that TRIM28 knockdown may be effective against NSCLC, and TRIM28 antibodies have the potential to act as novel diagnostic and therapeutic tools.