Di-μ-chlorido-bis­{[2-(2-pyridylmethyl­amino)ethanesulfonato-κ3 N,N′,O]copper(II)}

In the title compound, [Cu2(C8H11N2O3S)2Cl2], the Cu atoms are five-coordinated in a distorted square-pyramidal geometry by three donor atoms of the deprotonated anionic 2-(2-pyridylmethyl­amino)ethanesulfonate (pmt) ligand and two Cl atoms. The Cl atoms bridge two Cu atoms, giving a binuclear structure; the centroid of the Cu2Cl2 ring lies on a crystallographic center of inversion. The complex is stabilized by hydrogen bonds and π–π stacking inter­actions [average inter­planar distance = 3.4969 (1) Å and ring-centroid separation distance = 4.1068 (4) Å]

Role of NF-κB Activity in Apoptotic Response of Keratinocytes Mediated by Interferon-γ, Tumor Necrosis Factor-α, and Tumor-Necrosis-Factor-Related Apoptosis-Inducing Ligand

An important step in tumorigenesis involves loss of sensitivity to various apoptotic signals by malignant cells, imbuing them with an enhanced survival phenotype. NF-κB also regulates epidermal thickness, susceptibility to apoptosis, and tumor formation in skin. Keratinocytes were examined for their susceptibility to apoptosis using cytokines produced during an immunologic response to tumor antigens, i.e., interferon-γ and/or tumor necrosis factor-α (TNF-α). The role for NF-κB in this response was examined using a retroviral vector containing a degradation-resistant form of IκBα. Whereas interferon-γ and TNF-α either alone or in combination did not induce apoptosis in keratinocytes, after infection with the retrovirus to block NF-κB activation they became susceptible to TNF-α but not Fas-induced apoptosis. Moreover, when keratinocytes with repressed NF-κB activity were simultaneously treated with interferon-γ, there was a synergistic induction of apoptosis by TNF-α that was dependent on FADD, tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL), and caspase activation. Molecular abnormalities accompanying repressed NF-κB activity included failure to induce TNF-RII receptor together with enhanced levels of TRAIL death receptor 4. The ability of interferon-γ when combined with TNF-α to mediate keratinocyte apoptosis included induction of TRAIL coupled with diminished capacity of keratinocytes with repressed NF-κB activity to increase the TRAIL decoy receptor-1, as well as lower levels of several NF-κB-dependent antiapoptotic proteins accompanied by enhanced caspase 8 levels. These results indicate that interferon-γ and TNF-α synergistically induce keratinocyte apoptosis when concomitant induction of NF-κB is blocked. Participants in the apoptotic response mediated by NF-κB, besides cell-survival proteins, include modulation of TRAIL and both death and decoy receptors. Thus, not only does NF-κB signaling influence the intrinsic survival pathway for keratinocytes in normal skin, but it may also play a role in determining the apoptotic response to cytokines generated during an immune response via TRAIL produced by the keratinocytes themselves

Inhibitory effects of total saponins from Ilex pubescens Hook against hydrogen peroxide-induced cardiomyocyte apoptosis

Purpose: To study the protective effects of total saponins from Ilex pubescens Hook (IPTS) against cardiomyocyte apoptosis.Methods: Response surface methodology (RSM) based on Box-Benhnken Design (BBD) was carried out to optimize the extraction of IPTS. Thereafter, H9c2 cell model prepared by hydrogen peroxide (H2O2) treatment was used to investigate the effects of IPTS on cardiomyocyte apoptosis. Cell viability was determined using MTT assay, while the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), creatine kinase (CK) and catalase (CAT) were measured as indices of oxidative stress. Expressions of proteins related to apoptosis (caspase-3, Bax and Bcl-2) were measured using Western blot assay.Results: Optimal IPTS extraction was achieved with extraction temperature of 86.6 °C, extraction time of 2.23 h and water: raw material ratio of 10.8 mL/g. IPTS extract, at doses of 200, 400, 600 and 800 μg/mL, significantly increased the viability of H2O2-treated H9c2 cells (p < 0.05), but significantly decreased LDH and CK activities (p < 0.01). It also led to significant increases in SOD and CAT activities, and significant decreases in the levels of MDA in these cells (p < 0.01). There were significant down-regulation of the protein expressions of caspase-3 and Bax (p < 0.01) in IPTS-treated H9c2 cells, as well as significant up-regulation of Bcl-2 protein expression (p < 0.01).Conclusion: These results suggest that IPTS can protect cardiomyocytes against apoptosis via the inhibition of oxidative stress and mitochondria-induced intrinsic apoptosis.Keywords: Ilex pubescens, Total saponins, Cardiomyocytes, Apoptosis, H9c2 cell

Solvothermal synthesis of uniform bismuth nanospheres using poly(N-vinyl-2-pyrrolidone) as a reducing agent

Uniform bismuth nanospheres were successfully prepared from bismuth nitrate in the presence of poly(N-vinyl-2-pyrrolidone) (PVP) by solvothermal process. The product was characterized by powder X-ray diffraction, scanning electron microscopy, transmission electron microscopy, selected area electron diffraction, and energy-dispersive X-ray. PVP plays a critical role both as a reducing agent and a capping agent in the formation of bismuth nanospheres. Shape and size of bismuth nanospheres could be tuned by changing the employed PVP/bismuth salt ratio. It was also found the solvent had an effect on the morphologies of bismuth nanomaterials. The possible formation and growth mechanism of bismuth nanospheres were also discussed and proposed to explain the reduction step