Resveratrol derivatives potently induce apoptosis in human promyelocytic leukemia cells

Resveratrol has been shown to possess antioxidant and anticancer activities, but little is known on the effect of resveratrol derivatives. Recently we have isolated resveratrol and its dimers and trimers from peony (Paeonia lactiflora) seeds, and reported their strong antioxidant and cytotoxic activity. In the present study, we have evaluated cellular effects of resveratrol derivatives; viniferin, gnetin H, and suffruticosol B on the proliferation and apoptosis in HL-60 cells in vitro. All resveratrol and its derivatives reduced viability of HL-60 cells in a dose-dependent manner with their IC(50) values of 20-90 microM. Ascending orders of IC(50) values were suffruticosol B, gnetin H, viniferin and resveratrol respectively. HL-60 cells treated with the four stilbenes exhibited the distinct morphological changes characteristics of cell apoptosis such as chromatin condensation, apoptotic bodies, and DNA fragmentations. A time-dependent histogram of the cellular DNA analyzed by flow cytometry revealed a rapid increase in subdiploid cells and a concomitant decrease in diploid cells exposed to 100 microM resveratrol for 0-24 h. Cells treated with 25 microM of resveratrol, viniferin, gnetin H, and suffruticosol B for 24 h resulted in increment of sub-G1 population by 51, 5, 11 and 59%, respectively. Treatment of cells with 0-20 microM resveratrol for 5 h produced a concentration-dependent decrease in cytochrome P450 (CYP) 1B1 mRNA levels. Suffruticosol B also suppressed CYP1B1 gene expression. These results demonstrated that resveratrol oligomers also strongly suppressed HL-60 cell proliferation, and induced DNA damage. In addition, CYP1B1 gene supression may suggest an involvement in the resveratrol-induced apoptosis in HL-60 cells.     

Role of sphingomyelin-MAPKs pathway in heat-induced apoptosis

The role of sphingomyelinase (SMase) activation and mitogen activated protein kinases (MAPKs) activation in cellular apoptosis was investigated during the hyperthermic treatment of HL-60 human leukemia cells. Treating the cells for 1 h at 43(o)C caused more than 50% of cellular apoptosis within several hours. The neutral-SMase activity in the cells treated for 1 h at 42(o)C was slightly increased but decreased in the cells treated at 43(o)C or 44(o)C for the same period whereas the acid SMase activity was slightly increased after heating the cells at 42(o)C and 43(o)C and markedly increased at 44(o)C for 1 h. Treatment of cells with inhibitors of SMase activation and ceramide formation significantly reduced the heat-induced apoptosis. Three major families of mitogen-activated protein kinases (MAPKs), i.e. ERK1/2, p38 and JNK, were activated by the hyperthermic treatment of cells. Inhibition of ERK1/2 with PD98059 exerted little effect on the heat-induced apoptosis and p38 inhibition with SB203580 slightly lessened apoptosis whereas, inhibition of JNK with SP600125 markedly suppressed the heat-induced apoptosis. These results indicate that heat-shock induced the activation of SMase, particularly acid-SMase, thereby causing apoptosis and that JNK played a pivotal role in heat-induced apoptosis in HL-60 leukemia cells.     

Significant change in water contact angle of electrospray‐synthesized SiO2 films depending on their surface morphology

Amorphous SiO₂ films were deposited by means of an electrospray technique. The relation between the water contact angle (WCA) of the deposited SiO₂ films and the surface morphology is investigated. The feeding rate of the electrospray process greatly affects the morphology of the synthesized SiO₂ films. There is also a significant change in the WCA on the surface of the films: the rougher the surface, the greater the WCA. A model based on the Cassie–Baxter formulation is used to explain the change observed in the WCA on the SiO₂ films. Copyright © 2012 John Wiley & Sons, Ltd.     

Dispersion Stability of Fluorinated Multi-Walled Carbon Nanotubes in FC-27 Refrigerant

In order to achieve the dispersion stability of multi-walled carbon nanotubes (MWCNT) in a fluorinated refrigerant (FC-72) used in various cooling purposes, fluorinated MWCNT (MWCNT-F) was prepared by a combined process of oxidation and fluorination. As a fluorine source, (tridecafluoro-1,1,2,2-tetrahydrooctyl)trichlorosilane was used to react with hydroxyl groups on MWCNT (MWCNT-OH) generated by chemical oxidation. Pristine MWCNT, MWCNT-OH, and MWCNT-F were dispersed in FC-72 and MWCNT-F was also dispersed in polar and nonpolar solvents. The MWCNT-F has excellent colloidal stability in FC-72 because of the chemical affinity between FC-72 and functional groups (-CF_n) on the side walls of MWCNT. Through surface modifications, we could obtain the enhanced dispersion stability of MWCNT in a refrigerant. This homogenous MWCNT solution in FC-72 may be used to increase the heat transfer in FC-72 based nanofluids.     

Simultaneous quantification of ondansetron and tariquidar in rat and human plasma using a high performance liquid chromatography‐ultraviolet method

Ondansetron, a widely used antiemetic agent, is a P‐glycoprotein (P‐gp) substrate and therefore expression of P‐gp at the blood–brain barrier limits its distribution to the central nervous system (CNS), which was observed to be reversed by coadministration with P‐gp inhibitors. Tariquidar is a potent and selective third‐generation P‐gp inhibitor, and coadministration with ondansetron has shown improved ondansetron distribution to the CNS. There is currently no reported bioanalytical method for simultaneously quantifying ondansetron with a third‐generation P‐gp inhibitor. Therefore, we aimed to develop and validate a method for ondansetron and tariquidar in rat and human plasma samples. A full validation was performed for both ondansetron and tariquidar, and sample stability was tested under various storage conditions. To demonstrate its utility, the method was applied to a preclinical pharmacokinetic study following coadministration of ondansetron and tariquidar in rats. The presented method will be valuable in pharmacokinetic studies of ondansetron and tariquidar in which simultaneous determination may be required. In addition, this is the first report of a bioanalytical method validated for quantification of tariquidar in plasma samples.