Metal and Ligand Effects of Photoactive Transition Metal Carbonyls in the Iodine Degenerative Transfer Controlled Radical Polymerization and Block Copolymerization of Vinylidene Fluoride

The metal and ligand effect of a series of transition metal carbonyls in conjunction with alkyl and perfluoroalkyl halides was investigated in the initiation and control of the visible light, radical photopolymerizations of vinylidene fluoride (VDF) and respectively, in the synthesis of PVDF block copolymers. No polymerization was observed for CpMn­(CO)_3, CpCo­(CO)₂, Cp₂Fe₂(CO)_4, Cp*₂Cr₂(CO)_4, Mo­(CO)₆, Fe­(CO)_5, Cr­(CO)₆, Co₂(CO)₈, Co₄(CO)₁₂, Fe₃(CO)₁₂, Ru₃(CO)₁₂, (PPh₃)₂Ni­(CO)₂, Cp₂Ti­(CO)₂, and Au­(CO)­Cl. A free radical polymerization, and respectively an iodine degenerative transfer, controlled radical polymerization was obtained for Mn₂(CO)₁₀ ∼ Re₂(CO)₁₀ ≫ Cp₂Mo₂(CO)₆ ≫ Cp₂W₂(CO)₆ with CH₃(CH₂)₅–Br, CH₃(CH₂)₅–I, CH₃–I, CCl₃–Cl, CCl₃–Br, Br–(CF₂)₆–Br, and respectively with CF₃(CF₂)₃–I and I–(CF₂)_4,6–I. Furthermore, while Fe­(CO)₅, Cp*Cr₂(CO)₄ and Co₄(CO)₁₂ led to ∼ CF₂–I bond insertion, Re₂(CO)₁₀, Mn₂(CO)₁₀, Cp₂W₂(CO)₆, Cp₂Mo₂(CO)₆ and Cp₂Fe₂(CO)₄ provided quantitative radical activation of both PVDF–CH₂–CF₂–I and PVDF–CF₂–CH₂–I chain ends, and were employed in the synthesis of well-defined ABA triblock PVDF copolymers with vinyl acetate, <i>tert</i>-butyl acrylate, methyl methacrylate, isoprene, styrene, and acrylonitrile

Protective Effects of Lupeol against d‑Galactosamine and Lipopolysaccharide-Induced Fulminant Hepatic Failure in Mice

This study examined the hepatoprotective effects of lupeol (<b>1</b>, a major active triterpenoid isolated from <i>Adenophora triphylla</i> var. <i>japonica</i>) against d-galactosamine (GalN) and lipopolysaccharide (LPS)-induced fulminant hepatic failure. Mice were orally administered <b>1</b> (25, 50, and 100 mg/kg; dissolved in olive oil) 1 h before GalN (800 mg/kg)/LPS (40 μg/kg) treatment. Treatment with GalN/LPS resulted in increased levels of serum alanine aminotransferase, tumor necrosis factor (TNF)-α, and interleukin (IL)-6, as well as increased mortality, all of which were attenuated by treatment with <b>1</b>. In addition, levels of toll-like receptor (TLR)­4, myeloid differentiation primary response gene 88, TIR-domain-containing adapter-inducing interferon-β (TRIF), IL-1 receptor-associated kinase (IRAK)-1, and TNF receptor associated factor 6 protein expression were increased by GalN/LPS. These increases, except TRIF, were attenuated by <b>1</b>. Interestingly, <b>1</b> augmented GalN/LPS-mediated increases in the protein expression of IRAK-M, a negative regulator of TLR signaling. Following GalN/LPS treatment, nuclear translocation of nuclear factor-κB and the levels of <i>TNF-α</i> and <i>IL-6</i> mRNA expression increased, which were attenuated by <b>1</b>. Together, the present findings suggest that lupeol (<b>1</b>) ameliorates GalN/LPS-induced liver injury, which may be due to inhibition of IRAK-mediated TLR inflammatory signaling