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novel 2D sheet-like copper(II) complex formulated [Cu( trans-oxen)(μ-OH)(HO)]-(ClO)2nHO (1), where Hoxen is N, N'-bis(2-aminoethyl)oxamide, has been synthesized and characterized by elemental analysis, IR and UV-visible spectroscopy, and single-crystal X-ray diffraction. 1 crystallizes in triclinic space group P-1 with crystallographic data: a = 10.299(2) Å, b = 10.833(2) Å, c = 11.781(2) Å, α = 69.95(3)°, β = 81.10(3)°, γ = 62.44(3)°, and Z = 2. In the crystal structure, the cation [Cu( trans-oxen)(μ-OH)(HO)] exhibits a two-dimensional sheet-like structure for Cu(II) ions bridged both by trans-oxen and hydroxyl groups. Each Cu(II) ion is located in a slightly distorted square-pyramidal environment. The hydroxyl group bridges three [Cu(oxen)Cu] dications in which one oxen is μ-bridge while the other two act as never before reported μ-bridge. Perchlorate anions and HO molecules are inserted between the sheets and bridge the 2D cations via N-H···O and O-H···O hydrogen bonds to form an infinite three-dimensional system. The cyclic voltammetric behavior of 1 and the influence of counter ions on structure are preliminarily investigated. [ABSTRACT FROM AUTHOR]

Aim: To investigate the neuroprotective effect of propofol and its intracellular mechanism on neurons in vitro. Methods: Cell viability was determined with 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide reduction. Apoptotic cell death was determined by Hoechst 33258 staining and a fluorescence-activated cell sorter. The caspase-3 activity was measured by fluorometric assay. Mitogen-activated protein (MAP) kinase phosphorylation was detected with Western blotting. Results: The pretreatment of rat pheochromocytoma cell line PC12 with propofol (1-10 μmol/L) resulted in a significant recovery from hydrogen peroxide (H2O2)-induced cell death and the inhibition of H2O2 induced caspase-3 activation and PC12 cell apoptosis. Propofol inhibited the H2O2-induced p38 MAP kinase, but not c-Jun N-terminal kinase or extracellular signal-regulated kinase 1 and 2 activations. Conclusion: Propofol might attenuate H2O2-induced PC 12 cell death through the inhibition of signaling pathways mediated by the p38 MAP kinase. [ABSTRACT FROM AUTHOR]