Four bimetallic Al or Zn complexes supported by anilido-aldimine ligands (o-C6H4(NHAr)-CH=N)2CH2CH2 (Ar = 2,6-Me2C6H3,L1H2; Ar = 2,6-iPr2C6H3, L2H2) have been synthesized and characterized. Treatment of L1H2 or L2H2 with two equiv. of AlMe3 gives bimetallic complex L1(AlMe2)2 1 or L2 (AlMe2)2 2, respectively. Reaction of L1H2 or L2H2 with two equiv. of ZnEt2 leads to bimetallic complex L1(ZnEt)2 3 or L2(ZnEt)2 4, respectively. All of the complexes 1-4 are efficient catalysts for ring-opening polymerization of epsilon-caprolactone (CL) in the presence of benzyl alcohol and catalyze the polymerization of CL in living fashion yielding polymers with a narrow polydispersity index. The activity of bimetallic Zn complexes 3 and 4 is higher than bimetallic Al complexes 1 and 2.

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A number of Al complexes bearing bidentate N,N‐dialkylaniline–arylamido ligands, ortho‐(ArNCH2)C6H4NR2AlMe2 (R = Me, Ar = 2,6‐iPr2C6H3, 3a; 2,6‐Et2C6H3, 3b; 2,6‐Me2C6H3, 3c; 4‐MeC6H4, 3d; Ph, 3e; and R = Et, Ar = 2,6‐iPr2C6H3, 3f; 2,6‐Me2C6H3, 3g; Ph, 3h), have been synthesized from the reaction of the corresponding free ligands, ortho‐(ArNHCH2)C6H4NR2 (R = Me, Ar = 2,6‐iPr2C6H3, 2a; 2,6‐Et2C6H3, 2b; 2,6‐Me2C6H3, 2c; 4‐MeC6H4, 2d; Ph, 2e; and R = Et, Ar = 2,6‐iPr2C6H3, 2f; 2,6‐Me2C6H3, 2g; Ph, 2h), with AlMe3 (1 equiv.). All complexes were characterized by 1H and 13C NMR spectroscopy and elemental analysis. Single‐crystal X‐ray diffraction analysis of complexes 3c and 3e revealed that these Al complexes have a distorted tetrahedral geometry around the metal center. All complexes were found to be efficient catalysts for the ring‐opening polymerization of ϵ‐caprolactone (CL) in the presence of benzyl alcohol, and complexes 3a–h catalyze the polymerization of CL in a living fashion. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2009)

Lipopolysaccharide (LPS)-induced endothelial dysfunction plays an important role in the pathogenesis of cardiovascular diseases. LCZ696, the dual-acting angiotensin receptor blocker, and neprilysin inhibitor has been used for the treatment of heart failure with reduced ejection fraction. Recent work suggests that LCZ696 therapy might have an anti-inflammatory effect in cardiovascular tissue. In the current study, we show that LCZ696 attenuates LPS-induced oxidative stress by reducing the production of intracellular reactive oxygen species (ROS) and the measurements of malonyl dialdehyde (MDA) level in human umbilical vascular endothelial cells (HUVECs). LCZ696 inhibits LPS-induced expressions and secretions of the pro-inflammatory cytokines, interleukin-6 (IL-6), interleukin-1α (IL-1α), and tumor necrosis factor β (TNF-β) as well as the chemokines, monocyte chemotactic protein 1 (MCP-1), and chemokine (C-X-C motif) ligand 1 protein (CXCL1). Additionally, we found that LCZ696 reduces LPS-induced expressions of vascular cell adhesion molecule 1 (VCAM-1) and P-selectin and the attachment of U937 monocytes to HUVECs. Mechanistically, LCZ696 prevents LPS-induced activation of the TLR4/Myd88 pathway and nuclear translocation of nuclear factor kappa-B (NF-κB) p65 factor. Based on these findings, we conclude that LCZ696 is capable of ameliorating LPS-induced endothelial dysfunction via anti-inflammatory properties.