Organoborane Catalyzed Regioselective 1,4-Hydroboration of Pyridines

A bulky organoborane Ar^F₂BMe (Ar^F = 2,4,6-tris­(trifluoromethyl)­phenyl, <b>1</b>) has been synthesized. In C₆D₆ solution this organoborane and pyridine form a frustrated Lewis pair. Under mild conditions, <b>1</b> can efficiently catalyze 1,4-hydroboration of a series of pyridines. This reaction is highly chemo- and regioselective. The reaction intermediate, a boronium complex [Py₂Bpin]­[Ar^F₂B­(H)­Me] (<b>3</b>), was characterized in solution by NMR spectroscopy, which was also confirmed by DFT calculation

Supplemental material for Standard Reference Line Combined with One-Point Calibration-Free Laser-Induced Breakdown Spectroscopy (CF-LIBS) to Quantitatively Analyze Stainless and Heat Resistant Steel

<p>Supplemental material for Standard Reference Line Combined with One-Point Calibration-Free Laser-Induced Breakdown Spectroscopy (CF-LIBS) to Quantitatively Analyze Stainless and Heat Resistant Steel by Hongbo Fu, Huadong Wang, Junwei Jia, Zhibo Ni and Fengzhong Dong in Applied Spectroscopy</p

Synthesis and Reactivity of the CO₂ Adducts of Amine/Bis(2,4,6-tris(trifluoromethyl)phenyl)borane Pairs

Frustrated Lewis pairs (FLPs) comprised of bis­(2,4,6-tris­(trifluoromethyl)­phenyl)­borane (<b>1</b>) and a secondary amine (such as HN<i>i</i>Pr₂ or HNEt₂) readily react with CO₂ at room temperature to afford ammonium carbamatoborate salts <b>2</b>. When the reaction was carried out at 80 °C, carbamate boryl esters <b>3</b> were obtained with release of 1 equiv of H₂. The <i>i</i>Pr-substituted carbamate boryl ester <b>3a</b> can function as an intramolecular FLP to activate H₂, affording ammonium borylformate salt <b>4a</b> and formamide adduct <b>5a</b>. Two reaction pathways leading to the formation of <b>4a</b> and <b>5a</b> are proposed

Cardiac and lung α₂- AR levels and cardiac localization of α₂- AR subtypes in YHB or/and LPS-challenged mice.

<p>(A and B) Levels of α_2A, α_2B and α_2C-AR protein in the heart and lung (<i>n</i> = 8). LPS (20 mg/kg) or normal saline was injected intraperitoneally 1 h after intragastrical treatment with YHB (1 mg/kg) or water, the α_2A, α_2B and α_2C-AR proteins were determined using Western blotting at 4 h after LPS injection. *<i>P</i><0.05, **<i>P</i><0.01 compared with control group; ^#<i>P</i><0.05 compared with LPS group. (C) Representative confocal images of normal mouse cardiac sections. The sections were stained with antibodies against cardiac troponin I (blue), α₂-AR subtypes (green) and synaptophysin (SYP, a mark for presynaptic terminals, red) or CD34 (a marker for endothelial cells, red). Insets, high-power magnification of the area indicated by arrows. Scale bar = 20 µm.</p

Effects of YHB or/and reserpine (RSP) on the cardiomyocyte apoptosis in LPS-challenged mice.

<p>(A and B) Representative confocal images of cardiac troponin I, DAPI and TUNEL-stained cardiac sections are shown from LPS and YHB+LPS groups, respectively. (C) Apoptotic index (AI) of cardiomyocytes at 12 h after LPS injection (<i>n</i> = 10). (D) Cardiac caspase 3/7 activity at 2 h after LPS injection (<i>n</i> = 10). **<i>P</i><0.01 compared with control group; ^#<i>P</i><0.05, ^##<i>P</i><0.01 compared with LPS group.</p

Effects of YHB (1, 2 or 4 mg/kg) on cardiac and plasma TNF-α and NO levels in LPS-challenged mice.

<p>(A and B) Cardiac and plasma TNF-α levels were examined at 1 h after 20 mg/kg LPS challenge (<i>n</i> = 10). (C and D) Cardiac and plasma NO levels were determined at 12 h after 20 mg/kg LPS injection (<i>n</i> = 10). *<i>P</i><0.05, **<i>P</i><0.01 compared with control group; ^#<i>P</i><0.05, ^##<i>P</i><0.01 compared with LPS group.</p

Effects of Ber (1.0 µM) on DOX (1.0 µM) - induced a decrease in mitochondrial membrane potential and a rise in AMP/ATP ratio in neonatal rat cardiomyocytes.

<p>(A) Confocal images of JC-1 fluorescence. Mitochondrial membrane potential of the cardiomyocytes was measured by JC-1, an indicator mitochondrial function, in cardiomyocytes treated with Ber (1.0 µM) or/and DOX (1.0 µM) for 1 h, red fluorescence represents the mitochondrial aggregate JC-1and green fluorescence indicates the monomeric JC-1. (B) Graph represents the ratio of aggregated and monomeric JC-1, indicating changes in mitochondrial membrane potential (n = 5). *<i>P</i><0.001 compared with control group. ^#<i>P</i><0.05, ^{# #}<i>P</i><0.01 compared with DOX group. (C) Changes in AMP/ATP ratio in cardiomyocytes treated with Ber (1.0 µM) or/and DOX (1.0 µM) for 0.5 h, 1 h or 2 h (n = 3). *<i>P</i><0.05 compared with control group. ^#<i>P</i><0.05 compared with DOX group.</p

Effect of Ber on caspase activities, Bcl-2 protein level, cytoplasmic cytochrome c (Cyt c) and mitochondrial Bax contents in DOX-treated cardiomyocytes.

<p>(A, B and C) Cardiomyocytes were treated with DOX (1.0 µM) in the absence or presence of Ber (1.0 µM) for 12 h, caspase-3 (n = 4), caspase-8 (n = 4) and caspase-9 (n = 6) activity were analyzed by flow cytometry. (D, E and F) Cardiomyocytes were treated with DOX (1.0 µM) in the absence or presence of Ber (1.0 µM) for 6 h, levels of cytoplasmic Cyt c, mitochondrial Bax and Bcl-2 (whole cell homogenate) proteins were determined by Western blotting (n = 4). *<i>P</i><0.05, **<i>P</i><0.01 compared with control group. ^#<i>P</i><0.05, ^#^#<i>P</i><0.01 compared with DOX group.</p

Changes in phosphorylation of acetyl-CoA carboxylase (ACC), time course and dose-dependent alterations of AMPKα phosphorylation in neonatal rat cardiomyocytes treated with DOX or/and Ber.

<p>(A) Cardiomyocytes were pretreated with AMPK activator, 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) (0.5 mM), or vehicle for 90 min, and then incubated with DOX (1.0 µM) or/and Ber (1.0 µM) for 2 h, the Ser79 phosphorylation level of ACC, a downstream target of AMPK, was measured by Western blot assay (n = 4). (B and C) Time course of AMPKα phosphorylation. Cardiomyocytes were treated with DOX (1.0 µM) or/and Ber (1.0 µM) for 12 h (B) or 24 h (C), and AMPKα phosphorylation was examined by Western blot assay (n = 4). (D, E) Dose-dependent changes of AMPKα phosphorylation induced by DOX or Ber. Cardiomyocytes were treated with DOX (D, n = 3) or Ber (E, n = 4) at varying doses for 2 h, and Western blotting was performed to detect the AMPKα phosphorylation. *<i>P</i><0.05, **<i>P</i><0.01 compared with control group.^#<i>P</i><0.05 compared with DOX group.</p

Proposed mechanisms involved in improvement of LPS-induced cardiac dysfunction by YHB.

<p>Besides α₂ -AR in infiltrated macrophages, YHB blocked cardiac presynaptic α_2A-AR and in turn increases cardiac NE release during endotoxemia. Elevated cardiac NE inhibits cardiac TNF-α and iNOS expression, attenuates cardiomyocyte apoptosis via stimulating α₁-AR and β₂-AR, directly activates β₁-AR and thereby improves LPS-induced decreased EF.</p