Interconnectivity of Macroporous Hydrogels Prepared via Graphene Oxide-Stabilized Pickering High Internal Phase Emulsions.

Interconnected macroporous poly(acrylic acid) (PAA) hydrogels are prepared via oil-in-water (o/w) Pickering high internal phase emulsion (HIPE) templates stabilized by graphene oxide (GO). The amphiphilicity of GO is adjusted by slight modification with cetyltrimethylammonium bromide (CTAB). The morphology of macroporous PAA is observed by a field-emission scanning electron microscope (FE-SEM). The gas permeability is characterized to evaluate the interconnectivity of polymer foams. The pore and pore throat size can be tailored by varying the wettability and concentration of GO. The selective adsorption toward dyes of PAA hydrogels is proved. Macroporous PAA hydrogels with an open-cell structure show enhanced adsorption behavior of both methylene blue (MB) and copper(II) ions.

In vitro anticancer property of a novel thalidomide analogue through inhibition of NF-kappaB activation in HL-60 cells.

AIM: To investigate the anticancer property and possible mechanism of action of a novel sugar-substituted thalidomide derivative (STA-35) on HL-60 cells in vitro. METHODS: TNF-alpha-induced NF-kappaB activation was determined using a reporter gene assay. The MTT assay was used to measure cytotoxicity of the compound. The appearance of apoptotic Sub-G1 cells was detected by flow cytometry analysis. PARP cleavage and protein expression of NF-kappaB p65 and its inhibitor IkappaB were viewed by Western blotting. RESULTS: TA-35 (1-20 micromol/L) suppressed TNF-alpha-induced NF-kappaB activation in transfected cells (HEK293/pNiFty-SEAP) in a dose- (1-20 micromol/L) and time-dependent (0-48 h) manner. It was also shown that STA-35 exerted a dose-dependent inhibitory effect on HL-60 cell proliferation with an IC(50) value of 9.05 micromol/L. In addition, STA-35 induced apoptosis in HL-60 cells, as indicated by the appearance of a Sub-G1 peak in the cell cycle distribution, as well as poly ADP-ribose polymerase (PARP) cleavage. Subsequently, both NF-kappaB p65 and its inhibitor IkappaB gradually accumulated in cytoplasmic extracts in a dose- and time-dependent manner, indicating the blockage of NF-kappaB translocation induced by TNF-alpha from the cytoplasm to the nucleus. CONCLUSION: A novel sugar-substituted thalidomide derivative, STA-35, is potent toward HL-60 cells in vitro and induces apoptosis by the suppression of NF-kappaB activation.