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1.
Inorg Chem ; 60(11): 8181-8188, 2021 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-33983716

RESUMO

A series of N,O-coordinate iridium(III) complexes with a half-sandwich motif bearing Schiff base ligands for catalytic hydrogenation of nitro and carbonyl substrates have been synthesized. All iridium complexes showed efficient catalytic activity for the hydrogenation of ketones, aldehydes, and nitro-containing compounds using clean H2 as reducing reagent. The iridium catalyst displayed the highest TON values of 960 and 950 in the hydrogenation of carbonyl and nitro substrates, respectively. Various types of substrates with different substituted groups afforded corresponding products in excellent yields. All N,O-coordinate iridium(III) complexes 1-4 were well characterized by IR, NMR, HRMS, and elemental analysis. The molecular structure of complex 1 was further characterized by single-crystal X-ray determination.

2.
Inorg Chem ; 60(7): 5153-5162, 2021 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-33761239

RESUMO

Four air-stable cyclometalated half-sandwich iridium complexes 1-4 with C,N-donor Schiff base ligands were prepared through C-H activation in moderate-to-good yields. These complexes have been well characterized, and their exact structure was elaborated on by single-crystal X-ray analysis. The iridium(III) complexes 1-4 showed good catalytic activity in the imine synthesis under open-flask conditions (air as the oxidant) from primary amine oxidative homocoupling, secondary amine dehydrogenation, and the cross-coupling reaction of amine and alcohol. Substituents bonded on the ligands of the iridium complexes displayed little effect on the catalytic efficiency. The stability and good catalytic efficiency of the iridium catalysts, mild reaction conditions, and substrate universality showed their potential application in industrial production.

3.
Eur J Med Res ; 22(1): 12, 2017 Mar 28.
Artigo em Inglês | MEDLINE | ID: mdl-28351415

RESUMO

OBJECTIVE: To investigate the effect of carbonyl sulfide (COS) on limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) and the associated mechanism in rats. METHODS: ALI was induced by bilateral hind limb I/R in Sprague-Dawley (SD) rats. Sixty-four SD rats were randomly divided into the control group, I/R group, I/R + COS group, and I/R + AIR group. We observed the survival rate of the rats and the morphological changes of lung tissues, and we measured the change in the lung coefficient, the expression levels of the intercellular adhesion factor-1 (ICAM-1) protein in lung tissue, the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-lß, and interleukin (IL)-6 in both lung tissue and serum, and cell apoptosis. RESULTS: Limb I/R caused significant lung tissue damage. The number of polymorphonuclear neutrophil in alveolar septa, the expression level of the ICAM-1 protein in lung tissue, the expression levels of TNF-α, IL-1, and IL-6 in lung tissue and serum, the lung coefficient, and cell apoptosis all increased. When a low dose of COS gas was administered prior to limb I/R, the variation of the above indicators was significantly reduced, while an increase in the dose of COS did not reduce the lung injury but rather increased the mortality rate. CONCLUSION: Carbonyl sulfide is another new gaseous signaling molecule, and a low dose of exogenous COS may play a protective role in I/R-induced ALI by acting as an anti-inflammatory agent by promoting the production of antioxidants and by inhibiting the expression of adhesion molecule proteins.


Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Traumatismo por Reperfusão/tratamento farmacológico , Óxidos de Enxofre/administração & dosagem , Lesão Pulmonar Aguda/genética , Lesão Pulmonar Aguda/fisiopatologia , Animais , Apoptose/efeitos dos fármacos , Moléculas de Adesão Celular/genética , Extremidades/lesões , Extremidades/fisiopatologia , Humanos , Interleucina-6/genética , Masculino , Neutrófilos/efeitos dos fármacos , Neutrófilos/patologia , Ratos , Traumatismo por Reperfusão/fisiopatologia , Fator de Necrose Tumoral alfa/genética
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