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Schiff base {(E)‐4‐((2‐hydroxy‐3‐methoxybenzylidene)amino)‐1,5‐dimethyl‐2‐phenyl‐1,2‐dihydro‐3H‐pyrazol‐3‐one} was prepared by the condensation reaction between 2‐hydroxy‐3‐methoxybenzaldehyde and 4‐aminoantipyrine. In the process of forming the title complex, Schiff base was first coordinated with CuII ions to form the mononuclear CuII complex (abbreviated as the complex (I)). Next, Schiff base in the complex (I) removed a phenyl group and then changed from the amide to the iminol. The tautomer further formed the complex through the iminol oxygen, and the phenolic oxygen coordinated with metal ions (CuII and BiIII). The structure of the polynuclear CuIIBiIII complex (abbreviated as the complex (II)) was identified as [Bi2Cu6 L6O3] (L = C13H13N3O3) by elemental analysis, FT‐IR spectra, and single‐crystal X‐ray diffraction analysis. The antibacterial effect of Schiff base and its complex (II) were assessed on four bacterial strains involving gram‐positive strains (S. aureus and B. subtilis) and gram‐negative strains (E. coli and P. aeruginosa). The complex (II) exhibited stronger antibacterial activity than Schiff base. Assessment of cytotoxic activity against SNU‐16 cells (Human gastric cancer) has demonstrated that the complex (II) was more active than Schiff base, and their IC50 values were 0.29 and 1.83 μM, respectively. [ABSTRACT FROM AUTHOR]

A new bismuth(III) Schiff‐base complex [Bi2(HL)2(NO3)4] was synthesized by using equivalent molar of Schiff‐base ligand [H2L = (E)‐N′‐(2‐hydroxy‐3‐methoxybenzylidene)isonicotinohydrazide] and Bi(NO3)3•5H2O with the assistance of Mannitol. The complex was structurally characterized by elemental analysis, spectroscopic methods, and single crystal X‐ray diffraction. The experimental and theoretical vibrational bands (infrared and Raman spectra) have been discussed. The antimicrobial activity of the complex against Schizosaccharomyces pombe was evaluated by bio‐microcalorimetry at 32°C. Some thermokinetic parameters (k, Pmax, tG, and Qtotal) were obtained from the metabolic power–time curves of S. pombe, and their quantitative relationships with the concentration (c) were discussed. The half inhibition concentrations (IC50) of isoniazid, Schiff base, and the complex were calculated. The complex showed the strongest inhibition effect among three compounds. [ABSTRACT FROM AUTHOR]

In this study, a new Schiff base ligand [2-{[4-amino-5-(3,4,5-trimethoxy-benzyl)-pyrimidin-2-ylimino]-methyl}-6-methoxy-phenol, C22H24N4O5] and its bismuth(III) complex [BiC22H22N4O5Cl] were synthesized using o-vanillin and trimethoprim in anhydrous solvents. Chemical analysis, elemental analysis, spectrum analysis and TG-DSC analysis were employed to characterize the compositions and structures of the two new compounds. In particular, the metabolic thermogenic curves of Schizosaccharomyces pombe (S. pombe) and Helicobacter pylori (H. pylori) cells treated by the two new compounds at different concentrations were monitored by an isothermal microcalorimeter at 32.00 and 37.00 °C, respectively. On the basis of the metabolic thermogenic curves, some important biothermokinetic parameters such as the microbial growth rate constant (k), inhibition ratio (I) and half inhibition concentration (IC50) were estimated. The experimental results indicated that both the Schiff base ligand and its bismuth(III) complex could inhibit the growth metabolism of S. pombe and H. pylori, but the inhibitory abilities of the two compounds were as follows: the Schiff base ligand > the complex for S. pombe and the Schiff base ligand < the complex for H. pylori, respectively. More importantly, the results also found that the Schiff base bismuth(III) complex exhibited bidirectional biological effect and hormesis effect on H. pylori cell line, i.e., the complex can stimulate the growth metabolism of H. pylori at low concentration, while inhibiting its growth at high concentration. [ABSTRACT FROM AUTHOR]

Objective: Chronic stress is an important risk factor for atherosclerotic diseases. Our previous studies have shown that chronic unpredictable mild stress (CUMS) accelerates atherosclerosis and up-regulates TLR4/NF-κB expression in apoE-/- mice. However, TLR4/NF-κB signaling whether directly contributes to the development of atherosclerosis in CUMS mice is unclear. We hypothesized that the interference of TLR4/NF-κB can ameliorate CUMS-induced inflammation and atherosclerosis in apoE-/- mice. Methods: ApoE-/- mice were exposed to 12 weeks CUMS. Ad-siRNA TLR4 was given by tail vein injection (10 μl/mouse, every 5 days), and PDTC (an inhibitor of NF-κB) was given by intraperitoneal injection (60 mg/kg, once a day). Plasma corticosterone concentrations were determined by solid-phase 125I radioimmunoassay. Atherosclerosis lesions in aortic sinuses were evaluated and quantified by IMAGEPRO PLUS. Western blotting was used to detect the expression of TLR4, NF-κB, and IL-1β in aortas of the mice. Plasma lipid profiles, IL-1β, TNF-α, and MCP-1 were measured by ELISA. Results: Our results indicated that CUMS apoE-/- mice treatment with siRNA TLR4 significantly decreased atherosclerosis and down-regulated TLR4, NF-κB, and inflammatory cytokines. PDTC also remarkably reduced atherosclerosis and the levels of IL-1β, TNF-α and MCP-1 in plasma. However, Treatment with siRNA TLR4 or PDTC had no effect on plasma corticosterone levels, and lipid profiles. Conclusions: TLR4/NF-κB pathway may participate in CUMS-induced atherosclerosis through activation of proinflammatory cytokines in apoE-/- mice. Our data may provide a new potential therapeutic target for prevention of CUMS -induced atherosclerosis. [ABSTRACT FROM AUTHOR]